gmk_u_mouse.txt

GSE10000-GPL1261_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We previously observed that formation of aorta and innominate artery atherosclerotic lesions in the intima of hyperlipidemic apoE-deficient mice but not wild-type mice was accompanied by a marked age-dependent adventitial T cell infiltration. As the mice aged, adventitial T cells formed T/T cell-, T/B cell-, and T/B/dendritic cell aggregates adjacent to atherosclerotic lesions. Some of the adventitial infiltrates formed large clusters of various immune cells including T cells, B cells (centrocytes, follicular mantle cells), dendritic cells, follicular dendritic cells, and plasma cells with preferential formation in the suprarenal portion of the abdominal aorta. These data demonstrated that the immune lineage cell composition of atherosclerotic lesions and adventitia were distinct: The macrophage-foam cell-, T cell-, and SMC-dominated cell composition of atherosclerosis lesions versus the presence of immune cells capable of carrying out antigen-dependent T cell-driven humoral immune responses in the adventitia also indicated that immune reactions carried out in lesions or the adventitia are fundamentaly different. To distinguish between immunity-regulating genes in atherosclerosis lesions versus the adventitia, a combination of microarray profiling and laser capture microdissection was used. Stringent filters revealed 1163 differentially up-regulated probesets in apoE-/- mouse aortae at 78 weeks (w) versus 6 w. A fuzzy c-means cluster algorythm identified 2 clusters that significantly differed in their slope angles between time points: An apparent atherosclerosis cluster consisted of 771 probesets and an apparent adventitia cluster consisted of 392 probesets. Up-regulated genes at 32 w mirrored the influx of monocyte/macrophages into intima lesions whereas genes up-regulated between 32-78 w mirrored adventitial inflammation. To segregate both clusters into separate gene ontology (GO) molecular function groups, we determined statistically significant up-regulation (unpaired Student t-test; p < 0.05) between 6-32 w for the atherosclerosis cluster and between 32-78 w for the adventitia cluster. Among others, GO molecular function terms cytokine activity, cytokine binding, and immunoglobulin binding in the atherosclerosis cluster and cytokine activity, chemokine receptor activity, and antigen binding in the ATLO cluster suggested candidate genes in relation to inflammation triggered by macrophages or adventitia infiltration, respectively. Among other prototype atherosclerosis genes such as Itgax (complement receptor 4), Cd68, Lysz (lysozyme), Vcam1, and Icam1, the atherosclerosis cluster showed markedly overrepresented prototype macrophage/foam cell genes regulating inflammation in cytokine activity (GO: 0005125): Spp1 (osteopontin) and Il6; in cytokine binding (GO: 0019955) Cd74, Il10rb, Ccr2, and Ccr5; and in immunoglobulin binding (GO: 00119865) the proinflammatory galactose-binding lectin Lgals3, as well as genes in scavenger receptor activity and lipid transporter activity. By contrast, the adventitia cluster showed overrepresented genes regulating B cell recruitment, B cell maturation, germinal center formation, and autoimmunity in cytokine activity including Cxcl13, Ccl21, and Ltb, in CXC chemokine receptor activity the secondary lymphoid organ counterreceptor of CXCL13 Blr1 (also known as Cxcr5), Cxcr3, and Cxcr6; and in antigen binding several histocompatibility-2 loci and various markedly expressed immunoglobulin genes. As embryonic lymph node development and tertiary lymphoid organ neogenesis share common features signal intensities of genes specifying the GO molecular function term lymph node development (GO: 0048535) were examined in arrays prepared from wild-type and apoE-/- aortae. These results showed that Id2, Nfkb1, and Ltbr were constitutively expressed at significant levels in aortae of both mouse genotypes whereas other genes including Lta, Ltb, Glycam1, and the two lymphorganogenic genes Cxcl13 and Ccl21 were induced at 78 w in apoE-deficient aortae only. Thus, genes expressed by macrophage-foam cells and genes regulating ATLO neogenesis, embryonic lymph node development, or B cell maturation were constitutively expressed in the arterial wall in both genotypes or emerged in a stepwise fashion at 32 w and 78 w. To verify microarray signal intensity data, separate aortae extracts were examined by quantitative RT-PCR (QRT-PCR) analyses of wild-type and apoE-deficient mice at 32 and 78 w. These data showed that array signal values accurately reflected gene transcripts. Cell lineage analyses of the adventitial infiltrate and kinetic aorta microarray- and QRT-PCR analyses thus provided circumstantial evidence that immune responses in atherosclerosis intima lesions and the adventitia were distinct. To examine this possibility further, we selected areas of the abdominal aorta burdened with advanced lesions and separated lesions and corresponding adventitial infiltrates of 78 w old apoE-deficient mice by laser dissection microscopy. In addition, adventitiae of aorta segments that were not associated with adjacent lesions and adventitiae of wild-type mice were prepared. Consistent with the lack of a major adventitial leukocyte infiltration, wild-type adventitiae showed gene expression levels that were similar to lesion-free adventitiae of apoE-deficient mice indicating that atherosclerotic lesions directly affected adventitial inflammation in a segmental fashion. Stringent filter criteria identified genes that were differentially expressed in adventitiae and atherosclerotic lesions. Statistical analyses of overrepresented genes in GO molecular function or biological process groups were particularly instructive in cytokine activity, cytokine binding, antigen processing and presentation as well as in lymph node development. Thus, adventitiae in aorta segments with associated atherosclerotic lesions in cytokine activity showed overrepresentation of genes known to be associated with tertiary lymphoid organ formation including Cxcl13, Ccl21, and Ltb, whereas atherosclerotic lesions showed overrepresentation of prototype atherosclerosis-associated genes Ssp1 (osteopontin), Bmp4 (bone morphogenic protein 4), and Cxc3cl1 (fractalkine); in cytokine binding adventitiae showed overrepresentation of receptors implicated in B cell immunity and autoimmunity including Brl1 (counterreceptor for CXCL13), Ccr7, Tnfrsf4, and Cxcr3 whereas lesions showed overrepresentation of inflammatory mediator receptors including Tnfrs1b, Tgfbr1, and Il7r; moreover, in antigen processing and presentation, adventitiae showed overrepresentation of several histocompatibility loci; additional adventitial gene expression overrepresentations were observed in lymph node development (Fas, SpiB, Ltb, Flt3) whereas lesions showed expression of prototype macrophage genes including Tlr4, Tgfb1, and Tgfb2.  These data provide comprehensive topographical transcriptome information in adventitial tissue adjacent to atherosclerotic lesions versus lesions and are expected to form the basis for future cell lineage expression analyses using single cell detection methodology including ISH."'
GSE10000-GPL8321_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We previously observed that formation of aorta and innominate artery atherosclerotic lesions in the intima of hyperlipidemic apoE-deficient mice but not wild-type mice was accompanied by a marked age-dependent adventitial T cell infiltration. As the mice aged, adventitial T cells formed T/T cell-, T/B cell-, and T/B/dendritic cell aggregates adjacent to atherosclerotic lesions. Some of the adventitial infiltrates formed large clusters of various immune cells including T cells, B cells (centrocytes, follicular mantle cells), dendritic cells, follicular dendritic cells, and plasma cells with preferential formation in the suprarenal portion of the abdominal aorta. These data demonstrated that the immune lineage cell composition of atherosclerotic lesions and adventitia were distinct: The macrophage-foam cell-, T cell-, and SMC-dominated cell composition of atherosclerosis lesions versus the presence of immune cells capable of carrying out antigen-dependent T cell-driven humoral immune responses in the adventitia also indicated that immune reactions carried out in lesions or the adventitia are fundamentaly different. To distinguish between immunity-regulating genes in atherosclerosis lesions versus the adventitia, a combination of microarray profiling and laser capture microdissection was used. Stringent filters revealed 1163 differentially up-regulated probesets in apoE-/- mouse aortae at 78 weeks (w) versus 6 w. A fuzzy c-means cluster algorythm identified 2 clusters that significantly differed in their slope angles between time points: An apparent atherosclerosis cluster consisted of 771 probesets and an apparent adventitia cluster consisted of 392 probesets. Up-regulated genes at 32 w mirrored the influx of monocyte/macrophages into intima lesions whereas genes up-regulated between 32-78 w mirrored adventitial inflammation. To segregate both clusters into separate gene ontology (GO) molecular function groups, we determined statistically significant up-regulation (unpaired Student t-test; p < 0.05) between 6-32 w for the atherosclerosis cluster and between 32-78 w for the adventitia cluster. Among others, GO molecular function terms cytokine activity, cytokine binding, and immunoglobulin binding in the atherosclerosis cluster and cytokine activity, chemokine receptor activity, and antigen binding in the ATLO cluster suggested candidate genes in relation to inflammation triggered by macrophages or adventitia infiltration, respectively. Among other prototype atherosclerosis genes such as Itgax (complement receptor 4), Cd68, Lysz (lysozyme), Vcam1, and Icam1, the atherosclerosis cluster showed markedly overrepresented prototype macrophage/foam cell genes regulating inflammation in cytokine activity (GO: 0005125): Spp1 (osteopontin) and Il6; in cytokine binding (GO: 0019955) Cd74, Il10rb, Ccr2, and Ccr5; and in immunoglobulin binding (GO: 00119865) the proinflammatory galactose-binding lectin Lgals3, as well as genes in scavenger receptor activity and lipid transporter activity. By contrast, the adventitia cluster showed overrepresented genes regulating B cell recruitment, B cell maturation, germinal center formation, and autoimmunity in cytokine activity including Cxcl13, Ccl21, and Ltb, in CXC chemokine receptor activity the secondary lymphoid organ counterreceptor of CXCL13 Blr1 (also known as Cxcr5), Cxcr3, and Cxcr6; and in antigen binding several histocompatibility-2 loci and various markedly expressed immunoglobulin genes. As embryonic lymph node development and tertiary lymphoid organ neogenesis share common features signal intensities of genes specifying the GO molecular function term lymph node development (GO: 0048535) were examined in arrays prepared from wild-type and apoE-/- aortae. These results showed that Id2, Nfkb1, and Ltbr were constitutively expressed at significant levels in aortae of both mouse genotypes whereas other genes including Lta, Ltb, Glycam1, and the two lymphorganogenic genes Cxcl13 and Ccl21 were induced at 78 w in apoE-deficient aortae only. Thus, genes expressed by macrophage-foam cells and genes regulating ATLO neogenesis, embryonic lymph node development, or B cell maturation were constitutively expressed in the arterial wall in both genotypes or emerged in a stepwise fashion at 32 w and 78 w. To verify microarray signal intensity data, separate aortae extracts were examined by quantitative RT-PCR (QRT-PCR) analyses of wild-type and apoE-deficient mice at 32 and 78 w. These data showed that array signal values accurately reflected gene transcripts. Cell lineage analyses of the adventitial infiltrate and kinetic aorta microarray- and QRT-PCR analyses thus provided circumstantial evidence that immune responses in atherosclerosis intima lesions and the adventitia were distinct. To examine this possibility further, we selected areas of the abdominal aorta burdened with advanced lesions and separated lesions and corresponding adventitial infiltrates of 78 w old apoE-deficient mice by laser dissection microscopy. In addition, adventitiae of aorta segments that were not associated with adjacent lesions and adventitiae of wild-type mice were prepared. Consistent with the lack of a major adventitial leukocyte infiltration, wild-type adventitiae showed gene expression levels that were similar to lesion-free adventitiae of apoE-deficient mice indicating that atherosclerotic lesions directly affected adventitial inflammation in a segmental fashion. Stringent filter criteria identified genes that were differentially expressed in adventitiae and atherosclerotic lesions. Statistical analyses of overrepresented genes in GO molecular function or biological process groups were particularly instructive in cytokine activity, cytokine binding, antigen processing and presentation as well as in lymph node development. Thus, adventitiae in aorta segments with associated atherosclerotic lesions in cytokine activity showed overrepresentation of genes known to be associated with tertiary lymphoid organ formation including Cxcl13, Ccl21, and Ltb, whereas atherosclerotic lesions showed overrepresentation of prototype atherosclerosis-associated genes Ssp1 (osteopontin), Bmp4 (bone morphogenic protein 4), and Cxc3cl1 (fractalkine); in cytokine binding adventitiae showed overrepresentation of receptors implicated in B cell immunity and autoimmunity including Brl1 (counterreceptor for CXCL13), Ccr7, Tnfrsf4, and Cxcr3 whereas lesions showed overrepresentation of inflammatory mediator receptors including Tnfrs1b, Tgfbr1, and Il7r; moreover, in antigen processing and presentation, adventitiae showed overrepresentation of several histocompatibility loci; additional adventitial gene expression overrepresentations were observed in lymph node development (Fas, SpiB, Ltb, Flt3) whereas lesions showed expression of prototype macrophage genes including Tlr4, Tgfb1, and Tgfb2.  These data provide comprehensive topographical transcriptome information in adventitial tissue adjacent to atherosclerotic lesions versus lesions and are expected to form the basis for future cell lineage expression analyses using single cell detection methodology including ISH."'
GSE10010_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Control or IL-22-treated mouse colon in triplicate."'
GSE10029-GPL6328_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Genomic expression profiling of TNFalpha treated BDC2.5 diabetogenic CD4+ T Cells"'
GSE10029-GPL6328_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."'
GSE10029-GPL6328_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."'
GSE10029-GPL6328_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10029-GPL6328_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10029-GPL6328_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10029-GPL6329_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Genomic expression profiling of TNFalpha treated BDC2.5 diabetogenic CD4+ T Cells"'
GSE10029-GPL6329_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."'
GSE10029-GPL6329_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."'
GSE10029-GPL6329_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10029-GPL6329_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10029-GPL6329_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10029-GPL6330_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Genomic expression profiling of TNFalpha treated BDC2.5 diabetogenic CD4+ T Cells"'
GSE10029-GPL6330_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."'
GSE10029-GPL6330_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."'
GSE10029-GPL6330_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10029-GPL6330_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10029-GPL6330_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."'
GSE10071_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"NUP98-NSD1 links H3K36 methylation to Hox-A gene activation and leukaemogenesis"'
GSE10071_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Nuclear receptor-binding SET domain protein 1 (NSD1) prototype is a family of mammalian histone methyltransferases (NSD1, NSD2/MMSET/WHSC1, NSD3/WHSC1L1) that are essential in development and are mutated in human acute myeloid leukemia (AML), overgrowth syndromes, multiple myeloma and lung cancers. In AML, the recurring t(5;11)(q35;p15.5) translocation fuses NSD1 to nucleoporin-98 (NUP98). Here, we present the first characterization of the transforming properties and molecular mechanisms of NUP98-NSD1. We demonstrate that NUP98-NSD1 induces AML in vivo, sustains self-renewal of myeloid stem cells in vitro, and enforces expression of the HoxA7, HoxA9, HoxA10 and Meis1 proto-oncogenes. Mechanistically, NUP98-NSD1 binds genomic elements adjacent to HoxA7 and HoxA9, maintains histone H3 Lys 36 (H3K36) methylation and histone acetylation, and prevents EZH2-mediated transcriptional repression of the Hox-A locus during differentiation. Deletion of the NUP98 FG-repeat domain, or mutations in NSD1 that inactivate the H3K36 methyltransferase activity or that prevent binding of NUP98-NSD1 to the Hox-A locus precluded both Hox-A gene activation and myeloid progenitor immortalization. We propose that NUP98-NSD1 prevents EZH2-mediated repression of Hox-A locus genes by colocalizing H3K36 methylation and histone acetylation at regulatory DNA elements. This report is the first to link deregulated H3K36 methylation to tumorigenesis and to link NSD1 to transcriptional regulation of the Hox-A locus."'
GSE10082_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Conventional biochemical and molecular techniques identified previously several genes whose expression is regulated by the aryl hydrocarbon receptor (AHR). We sought to map the complete spectrum of AHR-dependent genes in male adult liver using expression arrays to contrast mRNA profiles in Ahr-null mice (Ahr–/–) with those in mice with wild-type AHR (Ahr+/+). Transcript profiles were determined both in untreated mice and in mice treated 19 h earlier with 1000 µg/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Expression of 456 ProbeSets was significantly altered by TCDD in an AHR-dependent manner, including members of the classic AHRE-I gene battery, such as Cyp1a1, Cyp1a2, Cyp1b1, and Nqo1. In the absence of exogenous ligand, AHR status alone affected expression of 392 ProbeSets, suggesting that the AHR has multiple functions in normal physiology. In Ahr–/– mice, only 32 ProbeSets exhibited responses to TCDD, indicating that the AHR is required for virtually all transcriptional responses to dioxin exposure in liver. The flavin-containing monooxygenases, Fmo2 and Fmo3, considered previously to be uninducible, were highly induced by TCDD in an AHR-dependent manner. The estrogen receptor alpha as well as two estrogen-receptor-related genes (alpha and gamma) exhibit AHR-dependent expression, thereby extending cross-talk opportunities between the intensively studied AHR and estrogen receptor pathways. p53 binding sites are over-represented in genes down-regulated by TCDD, suggesting that TCDD inhibits p53 transcriptional activity. Overall, our study identifies a wide range of genes that depend on the AHR, either for constitutive expression or for response to TCDD."'
GSE10082_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Conventional biochemical and molecular techniques identified previously several genes whose expression is regulated by the aryl hydrocarbon receptor (AHR). We sought to map the complete spectrum of AHR-dependent genes in male adult liver using expression arrays to contrast mRNA profiles in Ahr-null mice (Ahr–/–) with those in mice with wild-type AHR (Ahr+/+). Transcript profiles were determined both in untreated mice and in mice treated 19 h earlier with 1000 µg/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Expression of 456 ProbeSets was significantly altered by TCDD in an AHR-dependent manner, including members of the classic AHRE-I gene battery, such as Cyp1a1, Cyp1a2, Cyp1b1, and Nqo1. In the absence of exogenous ligand, AHR status alone affected expression of 392 ProbeSets, suggesting that the AHR has multiple functions in normal physiology. In Ahr–/– mice, only 32 ProbeSets exhibited responses to TCDD, indicating that the AHR is required for virtually all transcriptional responses to dioxin exposure in liver. The flavin-containing monooxygenases, Fmo2 and Fmo3, considered previously to be uninducible, were highly induced by TCDD in an AHR-dependent manner. The estrogen receptor alpha as well as two estrogen-receptor-related genes (alpha and gamma) exhibit AHR-dependent expression, thereby extending cross-talk opportunities between the intensively studied AHR and estrogen receptor pathways. p53 binding sites are over-represented in genes down-regulated by TCDD, suggesting that TCDD inhibits p53 transcriptional activity. Overall, our study identifies a wide range of genes that depend on the AHR, either for constitutive expression or for response to TCDD."'
GSE10082_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Conventional biochemical and molecular techniques identified previously several genes whose expression is regulated by the aryl hydrocarbon receptor (AHR). We sought to map the complete spectrum of AHR-dependent genes in male adult liver using expression arrays to contrast mRNA profiles in Ahr-null mice (Ahr–/–) with those in mice with wild-type AHR (Ahr+/+). Transcript profiles were determined both in untreated mice and in mice treated 19 h earlier with 1000 µg/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Expression of 456 ProbeSets was significantly altered by TCDD in an AHR-dependent manner, including members of the classic AHRE-I gene battery, such as Cyp1a1, Cyp1a2, Cyp1b1, and Nqo1. In the absence of exogenous ligand, AHR status alone affected expression of 392 ProbeSets, suggesting that the AHR has multiple functions in normal physiology. In Ahr–/– mice, only 32 ProbeSets exhibited responses to TCDD, indicating that the AHR is required for virtually all transcriptional responses to dioxin exposure in liver. The flavin-containing monooxygenases, Fmo2 and Fmo3, considered previously to be uninducible, were highly induced by TCDD in an AHR-dependent manner. The estrogen receptor alpha as well as two estrogen-receptor-related genes (alpha and gamma) exhibit AHR-dependent expression, thereby extending cross-talk opportunities between the intensively studied AHR and estrogen receptor pathways. p53 binding sites are over-represented in genes down-regulated by TCDD, suggesting that TCDD inhibits p53 transcriptional activity. Overall, our study identifies a wide range of genes that depend on the AHR, either for constitutive expression or for response to TCDD."'
GSE10082_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mice bearing wild-type or genetically deleted AHRs were treated with corn oil vehicle or TCDD, and their livers analyzed by expression arrays."'
GSE10093_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"For each group 4 female C57BL/6 mice were treated, spleen surgically removed and single cell suspensions generated. Cell suspensions were pooled, and CD8 positive T cells purified (purity > 99%). RNA was isolated using TRIzol and amplified using the Ambion message AMP kit. Target lableing and hybridization was performed using Affymetrix standard protocols"'
GSE10094_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Following infection with LCMV, CD4+ SMARTA TCR transgenic cells (specific for the gp61-80 epitope of the LCMV glycoprotein) rapidly expand, become effector cells, and go on to form a long-lived memory population.  Following infection with a recombinant Listeria monocytogenes expressing the LCMV epitope gp61-80, SMARTA cells also expand but display defective effector differentiation and fail to form memory.  In an attempt to understand the signals required for CD4 T cell memory differentiation, we compared gene expression by SMARTA cells at the peak of the primary response following either Lm-gp61 or LCMV infection."'
GSE10095_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"This study describes the application of a unique strategy to identify breast cancer antigens (TAA). In a mouse model, the strategy led to the identification of growth factor receptor-bound protein10 (Grb10) as a newly identified TAA. Grb10 is signal transduction molecule associated with multiple transmembrane tyrosine-kinase receptors. It was discovered by comparing microarrays of cellular breast cancer vaccines highly enriched for cells that induced breast cancer immunity in tumor-bearing mice, with non enriched vaccines."'
GSE10095_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The vaccines were prepared by transferring a cDNA expression library derived from SB5b cells, a breast cancer cell line (C3H/He origin (H-2k), into LM mouse fibroblasts (H-2k). As the transferred cDNA integrates spontaneously into the genome of the recipient cells, replicates as the cells divide, and is expressed, the vaccine could be prepared from microgram amounts of tumor tissue. Relatively few cells in the transduced cell-population, however, incorporated cDNA-fragments that included genes specifying TAA. (The vast majority specified normal cellular constituents.) A unique strategy was employed, therefore, to enrich the vaccine for immunotherapeutic cells. Twenty genes were over-represented in the enriched vaccines. One, the gene for Grb10, was approximately 100 fold over-represented. To determine if Grb10 in the enriched vaccine was partly responsible for its therapeutic benefits, the gene was transferred into the fibroblast cell line, which was then used as a vaccine. Mice with established breast cancer treated solely by immunization with the modified fibroblasts developed robust immunity to the breast cancer cells, which, in some instances, was sufficient to result in tumor-rejection."'
GSE10095_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"51Cr-release cytotoxicity assays. Mononuclear cells from the spleens of C3H/He mice immunized with the cDNA-transduced cells, or with cells transduced with a plasmid encoding the gene specifying Grb10, were isolated by Ficoll-Hypaque density gradient centrifugation. After washing, the cells were co cultured at 370 with mitomycin C-treated (45 min, 50 μg/ml) SB5b cells for 5 days (ratio of spleen cells:SB5b cells = 30:1). Afterward, the population that failed to adhere to the plastic cell culture flasks was collected and used as effector cells for the cytotoxicity determinations. Spleen cell mediated cytotoxicity was determined in a standard 51Cr-release assay, using 51Cr-labeled SB5b cells as targets in the reaction."'
GSE10095_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"The vaccine was prepared by transfer of a cDNA library derived from SB5b cells into the modified mouse fibroblasts. Since only a small proportion of the transduced cell population was expected to have incorporated cDNAs that included genes specifying tumor antigens (TAA), a unique strategy was used to enrich the vaccine for TAA-positive cells, as described previously (30). In brief, aliquots of the suspension of transduced cells were added to each of ten wells of a 96 well plate. Each pool contained a starting inoculum of 1 x 103 cells. Wells containing higher numbers of TAA-positive cells were detected by comparing the response of C3H/He mice to immunization with cells from the individual pools, as determined by both ELISPOT IFN-γ and 51Cr-release cytotoxicity assays. To obtain a sufficient number of cells for immunization, cells from the individual pools were allowed to increase to approximately 5 x 107, through periodic transfers to larger culture plates and eventually cell culture flasks. An aliquot of each of the expanded cell populations was maintained frozen/viable (for later recovery). The remaining portion was used for immunization. Frozen cells derived from the pool that stimulated immunity to the breast cancer cells to the greatest extent (immunohigh), and, for use as a control, from the pool that induced immunity to SB5b cells to the least extent (immunolow), were recovered, reestablished in culture and subjected to additional rounds of positive or negative immune selection (30). (As an additional control, one pool was not subjected to either positive or negative selection (master pool)). After five rounds of selection, microarrays were used to compare the gene expression profiles of cells in the immunohigh and immunolow pools."'
GSE10095_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The vaccine was prepared by transfer of a cDNA library derived from SB5b cells into the modified mouse fibroblasts. Since only a small proportion of the transduced cell population was expected to have incorporated cDNAs that included genes specifying tumor antigens (TAA), a unique strategy was used to enrich the vaccine for TAA-positive cells, as described previously (30). In brief, aliquots of the suspension of transduced cells were added to each of ten wells of a 96 well plate. Each pool contained a starting inoculum of 1 x 103 cells. Wells containing higher numbers of TAA-positive cells were detected by comparing the response of C3H/He mice to immunization with cells from the individual pools, as determined by both ELISPOT IFN-γ and 51Cr-release cytotoxicity assays. To obtain a sufficient number of cells for immunization, cells from the individual pools were allowed to increase to approximately 5 x 107, through periodic transfers to larger culture plates and eventually cell culture flasks. An aliquot of each of the expanded cell populations was maintained frozen/viable (for later recovery). The remaining portion was used for immunization. Frozen cells derived from the pool that stimulated immunity to the breast cancer cells to the greatest extent (immunohigh), and, for use as a control, from the pool that induced immunity to SB5b cells to the least extent (immunolow), were recovered, reestablished in culture and subjected to additional rounds of positive or negative immune selection (30). (As an additional control, one pool was not subjected to either positive or negative selection (master pool)). After five rounds of selection, microarrays were used to compare the gene expression profiles of cells in the immunohigh and immunolow pools."'
GSE10095_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Microarrays of cellular vaccines enriched for transduced fibroblasts that induced immunity to SB5b cells."'
GSE10117_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Nuclear factor of activated T-cells 5 (NFAT5) is a transcription factor that regulates hyperosmolarity-responsive genes and helps activated T lymphocytes adapt to and discharge their functions in hyperosmolar environments. We report here that the Rho-type guanine nucleotide exchange factor (GEF) Brx is essential for increased NFAT5 expression in response to osmotic stress in lymphoid tissues. Indeed, brx haploinsufficient mice expressed significantly less NFAT5 in their spleens than wild type controls and their splenocytes had a defective response to osmotic stress in vitro. Haploinsufficient mice also had smaller-sized spleens containing fewer splenocytes, as well as a defective immunoglobulin response to ovalbumin compared to wild type mice. The Brx GEF domain and the p38 mitogen-activated kinase (MAPK) cascade were both required for osmotic stress-mediated induction of NFAT5 in Jurkat cells. Brx physically interacted with the cJun kinase (JNK)-interacting protein (JIP) 4, a scaffold protein for activation of the p38 MAPK cascade that was required for osmotic stress-induced NFAT5 expression. Thus, Brx is a signal integrator for the adaptive response to osmotic stress in the immune system, activating small G proteins, attracting JIP4 and stimulating p38 MAPK, ultimately increasing the expression of NFAT5 and activating hyperosmolarity protective genes, a phenomenon crucial for proper immune function in hyperosmolar environments, such as inflammatory sites and immune organs."'
GSE10117_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Nuclear factor of activated T-cells 5 (NFAT5) is a transcription factor that regulates hyperosmolarity-responsive genes and helps activated T lymphocytes adapt to and discharge their functions in hyperosmolar environments. We report here that the Rho-type guanine nucleotide exchange factor (GEF) Brx is essential for increased NFAT5 expression in response to osmotic stress in lymphoid tissues. Indeed, brx haploinsufficient mice expressed significantly less NFAT5 in their spleens than wild type controls and their splenocytes had a defective response to osmotic stress in vitro. Haploinsufficient mice also had smaller-sized spleens containing fewer splenocytes, as well as a defective immunoglobulin response to ovalbumin compared to wild type mice. The Brx GEF domain and the p38 mitogen-activated kinase (MAPK) cascade were both required for osmotic stress-mediated induction of NFAT5 in Jurkat cells. Brx physically interacted with the cJun kinase (JNK)-interacting protein (JIP) 4, a scaffold protein for activation of the p38 MAPK cascade that was required for osmotic stress-induced NFAT5 expression. Thus, Brx is a signal integrator for the adaptive response to osmotic stress in the immune system, activating small G proteins, attracting JIP4 and stimulating p38 MAPK, ultimately increasing the expression of NFAT5 and activating hyperosmolarity protective genes, a phenomenon crucial for proper immune function in hyperosmolar environments, such as inflammatory sites and immune organs."'
GSE10134_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We employed a gene complementation strategy combined with microarray screening to identify miRNAs involved in the formation of erythroid (red blood) cells.  To search for GATA-1-regulated erythroid miRNAs, we used the Gata-1– erythroblast line G1E.  These cells proliferate in culture as immature erythroid precursors and undergo terminal maturation when GATA-1 activity is restored.  G1E-ER4 is a sub-line stably expressing an estrogen-activated form of GATA-1 (GATA-1 fused to the ligand binding domain of the estrogen receptor).  Treatment of G1E-ER4 cells with estradiol induces a GATA-1-regulated program of gene expression with concomitant cellular maturation.  We used a microarray to evaluate the expression of 292 different miRNAs in G1E-ER4 cells at 0 versus 24 hours after GATA-1 activation.  Affymetrix gene expression profiling has previously been deposited (GEO accession no. GSE628)."'
GSE10134_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"We employed a gene complementation strategy combined with microarray screening to identify miRNAs involved in the formation of erythroid (red blood) cells.  To search for GATA-1-regulated erythroid miRNAs, we used the Gata-1– erythroblast line G1E.  These cells proliferate in culture as immature erythroid precursors and undergo terminal maturation when GATA-1 activity is restored.  G1E-ER4 is a sub-line stably expressing an estrogen-activated form of GATA-1 (GATA-1 fused to the ligand binding domain of the estrogen receptor).  Treatment of G1E-ER4 cells with estradiol induces a GATA-1-regulated program of gene expression with concomitant cellular maturation.  We used a microarray to evaluate the expression of 292 different miRNAs in G1E-ER4 cells at 0 versus 24 hours after GATA-1 activation.  Affymetrix gene expression profiling has previously been deposited (GEO accession no. GSE628)."'
GSE10134_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Two condition experiment, 3 replicates each (independently grown and harvested) of untreated and estradiol-treated (24hrs) G1E-ER4 cells, which express an estrogen-responsive form of the GATA-1 transcription factor.  Each sample is compared to a common reference sample, comprised of an equal mixture of all 6 experimental samples."'
GSE10144-GPL1161_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The purpose of this study was to examine the effect of aldosterone receptor blockade on the immunopathogenesis and progression of nephritis in the (NZBxNZW) F1 murine lupus model. Female NZB/W F1 mice (11 weeks old) were treated daily with 25 or 50 mg/kg of oral spironolactone or vehicle. Proteinuria, renal function and serum autoantibody levels were monitored. Renal histopathology, immune complex deposition, and immunohistochemistry were analyzed at various time points. Targeted microarray analysis was performed on renal tissue, with subsequent real time PCR analysis of several differentially expressed genes."'
GSE10144-GPL6362_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The purpose of this study was to examine the effect of aldosterone receptor blockade on the immunopathogenesis and progression of nephritis in the (NZBxNZW) F1 murine lupus model. Female NZB/W F1 mice (11 weeks old) were treated daily with 25 or 50 mg/kg of oral spironolactone or vehicle. Proteinuria, renal function and serum autoantibody levels were monitored. Renal histopathology, immune complex deposition, and immunohistochemistry were analyzed at various time points. Targeted microarray analysis was performed on renal tissue, with subsequent real time PCR analysis of several differentially expressed genes."'
GSE10166_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Over-activation of the aryl hydrocarbon receptor by TCDD in mice leads among other phenotypes to a severe thymic atrophy accompanied by immunosuppression. TCDD causes a block in thymocyte maturation and a preferential emigration of immature CD4-CD8- DN thymocytes (recent thymic emigrants) into the periphery. As part of this study gene expression profiles from DN thymocytes and thymic emigrants were generated from TCDD and solvent control mice"'
GSE10168_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"AhR activation by TCDD in the ET, cortical epithelial cell line"'
GSE10168_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Over activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line."'
GSE10168_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"ET cells were grown to 80-90% confluence and treated with 5nM TCDD or solvent control (1,4-Dioxane, 0,05%V). 2h,4h and 6h after treatment, RNA was isolated using TRIzol and gene expression measured. All experiments wer done in biological duplicates."'
GSE10182_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"MDP- and Pam3CSK4-induced genes in naïve and tolerant macrophages"'
GSE10182_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The transcriptome induced via Nod2 stimulation is greatly expanded in TLR2-tolerant macrophages."'
GSE10182_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Genes induced by Pam3CSK4 or MDP were selected based on a three-fold increase over expression levels in unstimulated  macrophages.  Tolerized genes are defined as genes downregulated more than 2-fold in tolerant macrophages stimulated with  Pam3CSK4 or MDP."'
GSE10182_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Genes induced by Pam3CSK4 or MDP were selected based on a three-fold increase over expression levels in unstimulated  macrophages.  Tolerized genes are defined as genes downregulated more than 2-fold in tolerant macrophages stimulated with  Pam3CSK4 or MDP."'
GSE10192_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Rosiglitazone (Rosi), a member of the thiazolidinedione class of drugs used to treat type 2 diabetes, activates the adipocyte-specific transcription factor peroxisome proliferator-activated receptor gamma (PPARg). This activation causes bone loss in animals and humans, at least in part due to suppression of osteoblast differentiation from marrow mesenchymal stem cells (MSC). In order to identify mechanisms by which PPARg2 suppresses osteoblastogenesis and promotes adipogenesis in MSC, we have analyzed the PPARg2 transcriptome in response to Rosi. A total of 4,252 transcriptional changes resulted when Rosi (1 uM) was applied to the U-33 marrow stromal cell line, stably transfected with PPARg2 (U-33/g2), as compared to non-induced U-33/g2 cells. Differences between U-33/g2 and U-33 cells stably transfected with empty vector (U-33/c) comprised 7,928 transcriptional changes, independent of Rosi. Cell type-, time- and treatment-specific gene clustering uncovered distinct patterns of PPARg2 transcriptional control of MSC lineage commitment. The earliest changes accompanying Rosi activation of PPARg2 included adjustments in morphogenesis, Wnt signaling, and immune responses, as well as sustained induction of lipid metabolism. Expression signatures influenced by longer exposure to Rosi provided evidence for distinct mechanisms governing the repression of osteogenesis and stimulation of adipogenesis. Our results suggest interactions that could lead to the identification of a “master” regulatory scheme controlling osteoblast differentiation. "'
GSE10192_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Rosiglitazone (Rosi), a member of the thiazolidinedione class of drugs used to treat type 2 diabetes, activates the adipocyte-specific transcription factor peroxisome proliferator-activated receptor gamma (PPARg). This activation causes bone loss in animals and humans, at least in part due to suppression of osteoblast differentiation from marrow mesenchymal stem cells (MSC). In order to identify mechanisms by which PPARg2 suppresses osteoblastogenesis and promotes adipogenesis in MSC, we have analyzed the PPARg2 transcriptome in response to Rosi. A total of 4,252 transcriptional changes resulted when Rosi (1 uM) was applied to the U-33 marrow stromal cell line, stably transfected with PPARg2 (U-33/g2), as compared to non-induced U-33/g2 cells. Differences between U-33/g2 and U-33 cells stably transfected with empty vector (U-33/c) comprised 7,928 transcriptional changes, independent of Rosi. Cell type-, time- and treatment-specific gene clustering uncovered distinct patterns of PPARg2 transcriptional control of MSC lineage commitment. The earliest changes accompanying Rosi activation of PPARg2 included adjustments in morphogenesis, Wnt signaling, and immune responses, as well as sustained induction of lipid metabolism. Expression signatures influenced by longer exposure to Rosi provided evidence for distinct mechanisms governing the repression of osteogenesis and stimulation of adipogenesis. Our results suggest interactions that could lead to the identification of a “master” regulatory scheme controlling osteoblast differentiation. "'
GSE10192_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Rosiglitazone (Rosi), a member of the thiazolidinedione class of drugs used to treat type 2 diabetes, activates the adipocyte-specific transcription factor peroxisome proliferator-activated receptor gamma (PPARg). This activation causes bone loss in animals and humans, at least in part due to suppression of osteoblast differentiation from marrow mesenchymal stem cells (MSC). In order to identify mechanisms by which PPARg2 suppresses osteoblastogenesis and promotes adipogenesis in MSC, we have analyzed the PPARg2 transcriptome in response to Rosi. A total of 4,252 transcriptional changes resulted when Rosi (1 uM) was applied to the U-33 marrow stromal cell line, stably transfected with PPARg2 (U-33/g2), as compared to non-induced U-33/g2 cells. Differences between U-33/g2 and U-33 cells stably transfected with empty vector (U-33/c) comprised 7,928 transcriptional changes, independent of Rosi. Cell type-, time- and treatment-specific gene clustering uncovered distinct patterns of PPARg2 transcriptional control of MSC lineage commitment. The earliest changes accompanying Rosi activation of PPARg2 included adjustments in morphogenesis, Wnt signaling, and immune responses, as well as sustained induction of lipid metabolism. Expression signatures influenced by longer exposure to Rosi provided evidence for distinct mechanisms governing the repression of osteogenesis and stimulation of adipogenesis. Our results suggest interactions that could lead to the identification of a “master” regulatory scheme controlling osteoblast differentiation. "'
GSE10192_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"U-33/g2 and U-33/c cells were cultured in the presence or absence of Rosi and gene expression was monitored at three different time points (2, 24, 72h) after exposure to the agonist. Each time point corresponds to a separate stage of Rosi-treated U-33/g2 cell conversion from the osteoblast-like phenotype to the adipocyte-like phenotype and includes induction (2h), intermediate alterations in phenotype progression (24h), and a terminally differentiated adipocytic with completely suppressed osteoblastic phenotype (72h). The experiment is a full factorial design performed in replicate."'
GSE10192_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"U-33/g2 and U-33/c cells were cultured in the presence or absence of Rosi and gene expression was monitored at three different time points (2, 24, 72h) after exposure to the agonist. Each time point corresponds to a separate stage of Rosi-treated U-33/g2 cell conversion from the osteoblast-like phenotype to the adipocyte-like phenotype and includes induction (2h), intermediate alterations in phenotype progression (24h), and a terminally differentiated adipocytic with completely suppressed osteoblastic phenotype (72h). The experiment is a full factorial design performed in replicate."'
GSE10202_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Achieving a mechanistic understanding of disease and initiating preclinical therapeutic trials necessitate the study of huntingtin toxicity and its remedy in model systems. To allow the engagement of appropriate experimental paradigms, Huntington’s disease (HD) models need to be validated in terms of how they recapitulate a particular aspect of human disease. In order to examine transcriptome-related effects of mutant huntingtin, we compared striatal mRNA profiles from seven genetic mouse models of disease to that of postmortem human HD caudate using microarray analysis. Transgenic models expressing short N-terminal fragments of mutant huntingtin (R6/1 and R6/2 mice) exhibited the most rapid effects on gene expression, consistent with previous studies. Although changes in the brains of knock-in models of HD took longer to appear, 15-month and 22-month CHL2Q150/Q150, 18-month HdhQ92/Q92 and 2-year-old YAC128 animals also exhibited significant HD-like mRNA signatures. When the affected genes were compared across models, a robust concordance was observed. Importantly, changes concordant across multiple lines mice were also in excellent agreement with the mRNA changes seen in human HD caudate. Although it was expected that the expression of full-length huntingtin transprotein might result in unique gene expression changes compared to those caused by expression of an N-terminal huntingtin fragment, no discernable differences between full-length and fragment models were detected. There was, however, an overall concordance between transcriptomic signature and disease stage. We thus conclude that the transcriptional changes of HD can be modelled in several available lines of transgenic mice, comprising lines expressing both N-terminal and full-length mutant huntingtin proteins. The combined analysis of mouse and human HD transcriptomes provides an important chronology of mutant huntingtin's gene expression effects."'
GSE10210_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"Gene expression analysis of embryonic stem cells expressing VE-cadherin (CD144) during endothelial differentiation"'
GSE10210_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Endothelial differentiation occurs during normal vascular development in the developing embryo. Mouse embryonic stem (ES) cells were used to further define the molecular mechanisms of endothelial differentiation. By flow cytometry a population of VEGF-R2 positive cells was identified as early as 2.5 days after differentiation of ES cells, and a subset of VEGF-R2 + cells, that were CD41+ positive at 3.5 days.  A separate population of VEGF-R2+ stem cells expressing the endothelial-specific marker CD144 (VE-cadherin) was also identified at this same time point. Microarray analysis of >45,000 transcripts was performed on RNA obtained from cells expressing VEGF-R2, CD41, and CD144."'
GSE10210_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"We identified four populations of cells; cells expressing VEGF-R2 (day 2.5), CD41 expressing cells (day 3.5), cells expressing CD144 (VE-Cadherin, day 3.5), and cells expressing CD144 (day 6.5). In addition to this, we have also obtained the negative control cells at each time such as VEGF-R2 (day 2.5) negative, CD41 negative (day 3.5), CD144 negative (VE-Cadherin, day 3.5), and negative CD144 (day 6.5). RNA for the microarray experiments were obtained in duplicate from two separately conducted experiments using the murine embryonic stem cells.."'
GSE10218_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"In the present Experiment two different genotypes in combination with an established mouse tumor model were compared. An active form of the Sos (son of sevenless) is expressed under a keratin5 promoter leading to a constitutive activation of the Ras-Raf pathway, which results in skin papilloma formation. In the context of this tumor model an epidermis specific homozygote Fos-deletion was compared to homozygous floxed Fos-alleles. Both genotypes (Fos-deleted and Fos-floxed) were treated equally. The specimens were taken from skin papilloma at the mouse tail. A total number of six specimens from six different individuals (three biological replicates per genotype) were taken. Each sample was prepared and hybridized against Universal Mouse Reference RNA (Stratagene) in a dye-swap experiment, resulting in two technical replicates for each specimen, respectively."'
GSE10218_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"In the present Experiment two different genotypes in combination with an established mouse tumor model were compared. An active form of the Sos (son of sevenless) is expressed under a keratin5 promoter leading to a constitutive activation of the Ras-Raf pathway, which results in skin papilloma formation. In the context of this tumor model an epidermis specific homozygote Fos-deletion was compared to homozygous floxed Fos-alleles. Both genotypes (Fos-deleted and Fos-floxed) were treated equally. The specimens were taken from skin papilloma at the mouse tail. A total number of six specimens from six different individuals (three biological replicates per genotype) were taken. Each sample was prepared and hybridized against Universal Mouse Reference RNA (Stratagene) in a dye-swap experiment, resulting in two technical replicates for each specimen, respectively."'
GSE10224_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Microarray technology was used to assess the global gene expression profile of laser-microdissected motoneurons obtained by transplanted and veichle treated SMA, and wildtype mice."'
GSE10224_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"The microarray data derived from three different groups: wildtype controls (vehicle treated), transgenic SMA (vehicle treated) and transplanted SMA mice. Each population consists of three RNA profiling samples."'
GSE10235_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"In the central nervous system (CNS) the transcription factor NF-kappaB is a key regulator of inflammation and secondary injury processes. Following trauma or disease, the expression of NF-kappaB-dependent genes is activated, leading to both protective and detrimental effects on CNS recovery. Here we show that transgenic inactivation of astroglial NF-kappaB in mice (GFAP-IkappaBalpha-dn mice) resulted in dramatic reduction of disease severity and improvement in functional recovery following EAE. This coincided with a higher presence of leukocytes in the cord and brain of transgenic mice at the chronic phase of the disease, when the functional recovery over WT mice was the most significant. We observed that expression of proinflammatory genes in both spinal cord and cerebellum was delayed and reduced, while the loss of neuronal-specific molecules essential for synaptic transmission was limited compared to WT mice. Furthermore, death of retinal ganglion cells in affected retinas was almost abolished, suggesting the activation of neuroprotective mechanisms. Our data indicate that inhibiting NF-kappaB in astrocytes results in neuroprotective effects following EAE, directly implicating astrocytes in the pathophysiology of this disease."'
GSE10235_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"All mice used were 2-4 months old obtained by breeding heterozygous GFAP-IkappaBalpha-dn males with WT females. WT littermates were used as controls. Spinal cords from WT and GFAP-IkappaBalpha-dn transgenic mice (1), naive or induced with experimental autoimmune encephalomyelitis (EAE) at 10, 17 and 80 days post-induction (dpi) were used to isolate RNA. 3 animals were used for each time point."'
GSE10250_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Histone deacetylases (HDAC) are enzymes that modify key residues in histones to regulate chromatin architecture, and play a vital role in cell survival, cell cycle progression, and tumorigenesis. To understand the function of Hdac3, a critical component of the N-CoR/SMRT repression complex, a conditional allele of Hdac3 was engineered. Given the vital role of HDAC3 in normal cells and in the generation and treatment of various cancers, a conditional deletion of Hdac3 was engineered in mice. The deletion of Hdac3 in the germ line yielded very early embryonic lethality. Therefore, mouse embryonic-derived fibroblasts (MEFs) containing the Hdac3 conditional allele were used to examine the function of Hdac3 in cell viability and in cell cycle control. Given the links between Hdac3 and transcriptional repression, we used oligonucleotide micro arrays to examine RNA isolated from control and Cre recombinase expressing MEFs to define the changes in gene expression upon inactivation of Hdac3.  Initially, we compared RNA from Ad-Cre infected Hdac3FL/+ and Hdac3FL/- MEFs and then we extended the analysis to Hdac3FL/- MEFs expressing Cre-ER (tamoxifen responsive Cre-estrogen receptor fusion protein).  When the gene expression of ethanol-treated (vehicle) and tamoxifen-treated MEFs was compared at 72 hr post-induction, 83 genes were induced and 111 genes were down-regulated at least 1.5-fold upon inactivation of Hdac3.  Approximately, 48 genes were up-regulated in both Ad-Cre and tamoxifen-treated MEFs at the 72 hr time point.  The majority of the affected genes were associated with signal transduction and metabolism. Overall, few of the up-regulated genes at the 72hr time point in Ad-Cre and tamoxifen-treated MEFs are associated with apoptosis or with cell cycle control. Thus, these metabolic regulatory genes may be “core” Hdac3-regulated genes, and alterations in gene expression are unlikely to trigger apoptosis. "'
GSE10250_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Histone deacetylases (HDAC) are enzymes that modify key residues in histones to regulate chromatin architecture, and play a vital role in cell survival, cell cycle progression, and tumorigenesis. To understand the function of Hdac3, a critical component of the N-CoR/SMRT repression complex, a conditional allele of Hdac3 was engineered. Given the vital role of HDAC3 in normal cells and in the generation and treatment of various cancers, a conditional deletion of Hdac3 was engineered in mice. The deletion of Hdac3 in the germ line yielded very early embryonic lethality. Therefore, mouse embryonic-derived fibroblasts (MEFs) containing the Hdac3 conditional allele were used to examine the function of Hdac3 in cell viability and in cell cycle control. Given the links between Hdac3 and transcriptional repression, we used oligonucleotide micro arrays to examine RNA isolated from control and Cre recombinase expressing MEFs to define the changes in gene expression upon inactivation of Hdac3.  Initially, we compared RNA from Ad-Cre infected Hdac3FL/+ and Hdac3FL/- MEFs and then we extended the analysis to Hdac3FL/- MEFs expressing Cre-ER (tamoxifen responsive Cre-estrogen receptor fusion protein).  When the gene expression of ethanol-treated (vehicle) and tamoxifen-treated MEFs was compared at 72 hr post-induction, 83 genes were induced and 111 genes were down-regulated at least 1.5-fold upon inactivation of Hdac3.  Approximately, 48 genes were up-regulated in both Ad-Cre and tamoxifen-treated MEFs at the 72 hr time point.  The majority of the affected genes were associated with signal transduction and metabolism. Overall, few of the up-regulated genes at the 72hr time point in Ad-Cre and tamoxifen-treated MEFs are associated with apoptosis or with cell cycle control. Thus, these metabolic regulatory genes may be “core” Hdac3-regulated genes, and alterations in gene expression are unlikely to trigger apoptosis. "'
GSE10250_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Histone deacetylases (HDAC) are enzymes that modify key residues in histones to regulate chromatin architecture, and play a vital role in cell survival, cell cycle progression, and tumorigenesis. To understand the function of Hdac3, a critical component of the N-CoR/SMRT repression complex, a conditional allele of Hdac3 was engineered. Given the vital role of HDAC3 in normal cells and in the generation and treatment of various cancers, a conditional deletion of Hdac3 was engineered in mice. The deletion of Hdac3 in the germ line yielded very early embryonic lethality. Therefore, mouse embryonic-derived fibroblasts (MEFs) containing the Hdac3 conditional allele were used to examine the function of Hdac3 in cell viability and in cell cycle control. Given the links between Hdac3 and transcriptional repression, we used oligonucleotide micro arrays to examine RNA isolated from control and Cre recombinase expressing MEFs to define the changes in gene expression upon inactivation of Hdac3.  Initially, we compared RNA from Ad-Cre infected Hdac3FL/+ and Hdac3FL/- MEFs and then we extended the analysis to Hdac3FL/- MEFs expressing Cre-ER (tamoxifen responsive Cre-estrogen receptor fusion protein).  When the gene expression of ethanol-treated (vehicle) and tamoxifen-treated MEFs was compared at 72 hr post-induction, 83 genes were induced and 111 genes were down-regulated at least 1.5-fold upon inactivation of Hdac3.  Approximately, 48 genes were up-regulated in both Ad-Cre and tamoxifen-treated MEFs at the 72 hr time point.  The majority of the affected genes were associated with signal transduction and metabolism. Overall, few of the up-regulated genes at the 72hr time point in Ad-Cre and tamoxifen-treated MEFs are associated with apoptosis or with cell cycle control. Thus, these metabolic regulatory genes may be “core” Hdac3-regulated genes, and alterations in gene expression are unlikely to trigger apoptosis. "'
GSE10250_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Initially, we compared RNA from Ad-Cre infected Hdac3FL/+ and Hdac3FL/- MEFs. In this analysis, RNA isolated from 64hr and 72hr post Ad-Cre infection were used. We extended the analysis to Hdac3FL/- MEFs expressing Cre-ER (tamoxifen responsive Cre-estrogen receptor fusion protein). In this analysis, two different MEF preparations (repl1 and repl2), two different time points (64hr and 72hr) were used for array analysis with tamoxifen-treated MEFs. For vehicle (ethanol) treated MEFs, two different MEF preparations (repl1 and repl2), and a single timepoint (64hr) was used."'
GSE10250_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Initially, we compared RNA from Ad-Cre infected Hdac3FL/+ and Hdac3FL/- MEFs. In this analysis, RNA isolated from 64hr and 72hr post Ad-Cre infection were used. We extended the analysis to Hdac3FL/- MEFs expressing Cre-ER (tamoxifen responsive Cre-estrogen receptor fusion protein). In this analysis, two different MEF preparations (repl1 and repl2), two different time points (64hr and 72hr) were used for array analysis with tamoxifen-treated MEFs. For vehicle (ethanol) treated MEFs, two different MEF preparations (repl1 and repl2), and a single timepoint (64hr) was used."'
GSE10273_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Productive rearrangement of the immunoglobulin heavy chain locus triggers a major developmental checkpoint that promotes limited clonal expansion of pre-B cells, culminating in cell cycle  arrest and rearrangement of the kappa (κ) or lambda (λ) light-chain loci. B lineage cells lacking the related transcription factors IRF-4 and IRF-8 undergo a developmental arrest at the cycling pre-B cell stage and are blocked for light-chain recombination. Using Irf-4,8-/- pre-B cells we demonstrate that two pathways converge to synergistically drive light-chain rearrangement, a process that is not simply activated by cell cycle exit. One pathway is directly dependent on IRF-4, whose expression is elevated by pre-BCR signaling.  IRF-4 targets the κ 3′ and λ enhancers to increase locus accessibility and positions a kappa allele away from pericentromeric heterochromatin. The other pathway is triggered by attenuation of IL-7 signaling and results in activation of the κ intronic enhancer via binding of the transcription factor, E2A. Intriguingly, IRF-4 regulates the expression of CXCR4 and promotes the migration of pre-B cells in response to the chemokine CXCL12. We propose that IRF-4 coordinates the two pathways regulating light-chain recombination by positioning pre-B cells away from IL-7 expressing stromal cells."'
GSE10273_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Productive rearrangement of the immunoglobulin heavy chain locus triggers a major developmental checkpoint that promotes limited clonal expansion of pre-B cells, culminating in cell cycle  arrest and rearrangement of the kappa (κ) or lambda (λ) light-chain loci. B lineage cells lacking the related transcription factors IRF-4 and IRF-8 undergo a developmental arrest at the cycling pre-B cell stage and are blocked for light-chain recombination. Using Irf-4,8-/- pre-B cells we demonstrate that two pathways converge to synergistically drive light-chain rearrangement, a process that is not simply activated by cell cycle exit. One pathway is directly dependent on IRF-4, whose expression is elevated by pre-BCR signaling.  IRF-4 targets the κ 3′ and λ enhancers to increase locus accessibility and positions a kappa allele away from pericentromeric heterochromatin. The other pathway is triggered by attenuation of IL-7 signaling and results in activation of the κ intronic enhancer via binding of the transcription factor, E2A. Intriguingly, IRF-4 regulates the expression of CXCR4 and promotes the migration of pre-B cells in response to the chemokine CXCL12. We propose that IRF-4 coordinates the two pathways regulating light-chain recombination by positioning pre-B cells away from IL-7 expressing stromal cells."'
GSE10285_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Gene expression of Ethanol-treated hepatocytes from WT and transglutaminase 2 knockout mice"'
GSE10285_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Non or 100mM Ethanol-treated WT hepatocytes, Non or 100mM Ethanol-treated TG2KO hepatocytes."'
GSE10290_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Beyond demonstrating a critical role for progesterone receptor signaling in normal mammary epithelial proliferation, the progesterone receptor knockout mouse disclosed the progesterone receptor along with its effector pathways as key determinants of mammary neoplastic progression.  Despite these advances, however, further progress in our mechanistic understanding of progesterone’s involvement in mammary morphogenesis and tumorigenesis is contingent upon defining the essential effector pathways responsible for transducing the progesterone signal into a mammary proliferative and/or pro-survival response.  Toward this goal, a judiciously chosen acute progesterone treatment regimen together with microarray methods was applied to the mammary gland of the normal mouse to uncover new effectors that operate immediately downstream of the progesterone mammary signal.  Examination of the resultant progesterone-responsive transcriptome disclosed “inhibitor of differentiation or DNA binding 4” (Id4) as a molecular target acutely induced by progesterone in the murine mammary epithelium."'
GSE10290_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Microarray analysis was performed on mammary tissue total RNA obtained from ovariectomized mice previously treated with progesterone for 4, 16, 28, and 76 hours.  For each hormone treatment time-point, mammary gland microarray data from sesame oil (vehicle) treated mice was included as controls.  Total mammary gland RNA from each time-point and treatment group was interrogated using the Affymetrix GeneChip Mouse Genome 430 2.0 Array.  For a given time-point and treatment group, three sets of mice (5 mice in each set) were used for gene expression profiling; mammary RNA pooled from each set was hybridized to one microarray chip.  Therefore, a total of 15 mice (or 3 microarray chips) were used per time-point and treatment group."'
GSE10291_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"To gain insights into the molecular mechanisms of oligodendrocyte differentiation, we performed microarray expression profiling of the oligodendroglial cell line, Oli-neu, treated with the Rho kinase (ROCK) inhibitor, Y-27632 or with conditioned neuronal medium. This resulted in the identification of the transmembrane protein 10 (Tmem10/Opalin), a novel type I transmembrane protein enriched in differentiating oligodendrocytes. In primary cultures, Tmem10 was abundantly expressed in O4-positive oligodendrocytes, but not in oligodendroglial precursor cells, astrocytes, microglia or neurons. In mature oligodendrocytes Tmem10 was enriched in the rims and processes of the cells and was only found to a lesser extent in the membrane sheets."'
GSE10291_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"2. olineu in presence of neurons (control) vs. Y27631 treated olineu in presence of neurons"'
GSE10297_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Leptin, a hormone produced primarily by adipose tissue, plays a role in both energy homeostasis and reproduction, and is required in early pregnancy.  Leptin stimulates metalloproteinase activity in cultured human trophoblast and stimulates invasiveness of cultured mouse trophoblast.  The goal of the present study was to examine molecular mechanisms of this function in primary cultures of mouse trophoblast.  Leptin was found to stimulate the phosphorylation of MEK, but not STAT3.. It also increased levels of the protein SOCS3.  The ability of leptin to stimulate metalloproteinase activity was blocked by the MEK inhibitor PD98059, but also by the vehicle inhibitor DMSO.  Microarray analysis revealed that leptin stimulated some genes associated with cell motility, such as Stmn1.  In addition, leptin appeared to inhibit changes in gene expression associated with terminal differentiation of trophoblast giant cells, including inhibition of members of the TGFß signaling pathway and of genes associated with endoreduplication.  However, feulgen staining revealed a loss of cells with low ploidy.  We conclude that leptin may be promoting trophoblast invasion by maintaining cells in an intermediate stage of differentiation."'
GSE10312_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"This study focuses on the impact of developmental Pb exposure on splenic gene expression. Pb exposure from gestational day 8 (gd8) to post-natal day 21 (pnd21) was used to obtain insight into how Pb induces anemia and negatively influences the immune response"'
GSE10312_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Keywords: exposure analysis"'
GSE10312_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"This study uses Codelink Mouse whole genome microarrays. Mouse spleen from 3 control and 3 experimental (treated with 0.1mM Pb since gd8) BALB/c female mice on pnd21 were used to study gene expression."'
GSE10318_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Methods and Results: We analyzed mice ectopically expressing Tbx3 in the atrial myocardium by genome-wide microarray and expression analysis. We found a prominent role for Tbx3 in defining the nodal phenotype by repressing working myocardial genes (sarcomeric, mitochondrial, fast conduction) and cell proliferation regulators, and in inducing node-associated genes. Moreover, there was a striking induction of genes associated with endocardial cushions and mesenchyme. Using gain-of-function models, we found that in the developing heart both Tbx2 and Tbx3 induce ectopic Bmp2 and Tgfb2 expression and endocardial cushion formation. Analysis of compound Tbx2/Tbx3 mutant embryos revealed that upon loss of more than two functional alleles, expansion of the AV myocardium does not occur and AV cushions fail to form."'
GSE10318_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"Nppa-Cre4 (Cre4) mice were crossed with CT mice to obtain efficient activation of Tbx3 in atria of double transgenic Cre4-CT mice, as previously described (Hoogaars et al., 2007). To investigate the gene expression profile of atria of Cre4-CT mice, we performed whole genome microarray analysis using Sentrix Mouse-6 oligonucleotide beadchips."'
GSE10341_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The catecholamine norepinephrine is required for fetal survival, but its essential function is unknown.  When catecholamine-deficient [tyrosine hydroxylase (Th) null] mouse fetuses die at E13.5-E14.5, they resemble wild type fetuses exposed to hypoxia. They exhibit bradycardia (28% reduction in heart rate), thin ventricular myocardium (20% reduction in tissue), epicardial detachment, and death with vascular congestion, hemorrhage and edema. At E12.5, prior to the appearance of morphological deficits associated with Th deletion, catecholamine-deficient fetuses are preferentially killed by experimentally-induced hypoxia and have lower tissue pO2 than wild type siblings.  Catecholamine-deficient fetuses also induced HIF-1 target genes to a greater extent than wild type siblings, supporting the notion that null fetuses experience greater hypoxia or have an enhanced response to hypoxia. Hypoxia induces a 13-fold increase in plasma norepinephrine levels, which would be expected to increase heart rate, thereby, improving oxygen delivery in wild type mice. Surprisingly, increasing maternal oxygen (FiO2 33% or 63%) prevents the effects of catecholamine-deficiency, restoring heart rate, myocardial mass and survival of Th null fetuses.  We suggest that norepinephrine mediates fetal survival by maintaining oxygen homeostasis as vulnerability to constitutive hypoxia increases as fetal growth accelerates during normal development."'
GSE10343_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"With advances in supportive therapy in the last two decades, mortality rates from ALI/ARDS have improved somewhat, but remain around 30 to 40% with significant morbidity in survivors. Several promising treatments are in various stages of evaluation, but many have failed to prove beneficial in large randomized clinical trials (RCT). The first definitive step forward in ALI therapeutics occurred recently as a result of a large RCT demonstrating a mortality decrease from 40 to 31% with the use of low-volume ventilation strategies. From this, it is clear that the opportunity for successful intervention in ALI exists. However, therapeutic advances remain frustrated by the lack of complete understanding of ALI pathophysiology. This stresses the importance of integrating basic and clinical research of the molecular pathogenesis of this disease. The conclusions of a recent National Heart, Lung, and Blood Institute (NHLBI) Working Group on ALI support this type of research as a priority for future investigations of ALI. One of the areas of research given priority by this ALI Working Group is the issue of ALI severity progression and the role of cells of innate immunity in this process. Currently, the processes that determine which ALI patients progress to ARDS and which do not are unclear. As with many phenotype differences, there is most likely a genetic component involved. The basis for this has been demonstrated. For example, a surfactant protein B (SP-B) polymorphism appears to increase a patient’s risk of developing ALI from pneumonia. Additionally, a polymorphism in the promoter region of the gene for interleukin-6 (IL-6) has been associated with a poor prognosis in patients with ARDS. Understanding the intracellular processes of these genes and the cells expressing them in ALI progression could lead to the identification of molecular markers of ALI severity and eventually to the development of targeted therapies. An examination of genetically uniform animals will provide a clearer insight into the interaction between immune cells in ALI progression as well as guide future human experiments."'
GSE10343_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Specific Aim 1. We will prospectively collect and bank RNA from peripheral blood CD4+ T lymphocytes (Th1 and Th2 subsets) and platelets from cecal ligation and puncture-treated BALB/c mice using a negative selection technique. Specific Aim 2. Four mice will undergo whole blood sampling at each of 3 time points (t = 0, 24, and 48 hours). Time 0 represents the point of CLP. Specific Aim 3. The temporal series of 3 cell types pooled within each time point will be expression profiled (3 time points x 3 cell types x MOE430A array = 9 profiles) in order to generate a map of potential cell-cell interactions and a prioritization model for examining these further."'
GSE10347_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Hexose-6-phosphate dehydrogenase (H6PD)is the initial component of a pentose phosphate pathway inside the endoplasmic reticulum (ER) that generates NADPH for ER enzymes. In liver, H6PD is required for the 11-oxoreductase activity of 11ss-hydroxysteroid dehydrogenase type 1 (11ss-HSD1), which converts inactive 11-oxo glucocorticoids to their active 11-hydroxyl counterparts; consequently, H6PD null mice are relatively insensitive to glucocorticoids, exhibiting fasting hypoglycemia, increased insulin sensitivity despite elevated circulating levels of corticosterone, and increased basal and insulin-stimulated glucose uptake in muscles normally enriched in Type II (fast) fibers which have increased glycogen content. They also display a progressive vacuolar myopathy evident after 4 weeks of age."'
GSE10389-GPL81_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"STAT5A and STAT5B proteins belong to the family of signal transducers and activators of transcription. They are encoded by 2 separate genes with 91% identity in their amino acid sequences. Despite their high degree of conservation, STAT5A and STAT5B exert non-redundant functions, resulting at least in part from differences in target gene activation. To better characterize the differential contribution of STAT5A and STAT5B in gene regulation, we performed single or double knock-down of STAT5A and STAT5B using small interfering RNA. Subsequent gene expression profiling and RT-qPCR analyses of IL-3-stimulated Ba/F3-beta cells led to the identification of putative novel STAT5 target genes. Chromatin immunoprecipitation assays analyzing the corresponding gene loci identified unusual STAT5 binding sites compared to conventional STAT5 responsive elements. Some of the STAT5 targets identified are upregulated in several human cancers, suggesting that they might represent potential oncogenes in STAT5-associated malignancies."'
GSE10389-GPL81_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"STAT5A and STAT5B proteins belong to the family of signal transducers and activators of transcription. They are encoded by 2 separate genes with 91% identity in their amino acid sequences. Despite their high degree of conservation, STAT5A and STAT5B exert non-redundant functions, resulting at least in part from differences in target gene activation. To better characterize the differential contribution of STAT5A and STAT5B in gene regulation, we performed single or double knock-down of STAT5A and STAT5B using small interfering RNA. Subsequent gene expression profiling and RT-qPCR analyses of IL-3-stimulated Ba/F3-beta cells led to the identification of putative novel STAT5 target genes. Chromatin immunoprecipitation assays analyzing the corresponding gene loci identified unusual STAT5 binding sites compared to conventional STAT5 responsive elements. Some of the STAT5 targets identified are upregulated in several human cancers, suggesting that they might represent potential oncogenes in STAT5-associated malignancies."'
GSE10389-GPL81_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Ba/F3-beta cells transfected with either control (scramble I) or Stat5A and Stat5B siRNAs were stimulated with IL-3 for either 30 minutes or 2 hours.  Unstimulated Ba/F3-beta cells transfected with scramble I siRNA were used as a control. "'
GSE10389-GPL81_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Total RNA was isolated using the RNeasy Maxi kit, including an on-column DNase I treatment to eliminate genomic DNA contamination, according to the manufacturer’s protocol (Qiagen, Valencia, CA). DNase-treated total RNA (5 µg) was synthesized into biotinylated cRNA probe using one-cycle target labeling and IVT labeling (Affymetrix, Inc., Santa Clara, CA) according to manufacturer’s instructions. Fifteen µg of biotinylated cRNA probe from each sample was hybridized onto murine U74A, U74B, U74C Affymetrix Microarray chips. The hybridized chips were then washed using the Affymetrix GeneChip Fluidics 400 station and scanned in the Affymetrix GeneChip Scanner 3000 (Affymetrix, Inc., Santa Clara, CA) according to manufacturer’s instructions.  The quality of cRNA probe synthesis and efficiency of hybridization was analyzed in the GeneChip Operating System for each Affymetrix chip once scanning was complete. Microarray data were normalized using MAS5 and then analyzed using the Genespring (Agilent, Palo Alto, CA). "'
GSE10389-GPL81_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Out of the 36,767 genes, 14,553 passed our noise and P/M/A call filters. Genes were further selected for being stimulated at least 2-fold by IL-3 after 30 minutes (164 genes) and 2 hours (553 genes) stimulation compared to the unstimulated cells (ScI-transfected cells). Then, IL-3 induced genes that were down-regulated at least 2-fold in the STAT5A/B siRNA-transfected cells at 30 minutes and 2 hours (12 and 29 respectively) were identified as putative STAT5 target genes and further investigated. "'
GSE10389-GPL81_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Out of the 36,767 genes, 14,553 passed our noise and P/M/A call filters. Genes were further selected for being stimulated at least 2-fold by IL-3 after 30 minutes (164 genes) and 2 hours (553 genes) stimulation compared to the unstimulated cells (ScI-transfected cells). Then, IL-3 induced genes that were down-regulated at least 2-fold in the STAT5A/B siRNA-transfected cells at 30 minutes and 2 hours (12 and 29 respectively) were identified as putative STAT5 target genes and further investigated. "'
GSE10389-GPL82_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"STAT5A and STAT5B proteins belong to the family of signal transducers and activators of transcription. They are encoded by 2 separate genes with 91% identity in their amino acid sequences. Despite their high degree of conservation, STAT5A and STAT5B exert non-redundant functions, resulting at least in part from differences in target gene activation. To better characterize the differential contribution of STAT5A and STAT5B in gene regulation, we performed single or double knock-down of STAT5A and STAT5B using small interfering RNA. Subsequent gene expression profiling and RT-qPCR analyses of IL-3-stimulated Ba/F3-beta cells led to the identification of putative novel STAT5 target genes. Chromatin immunoprecipitation assays analyzing the corresponding gene loci identified unusual STAT5 binding sites compared to conventional STAT5 responsive elements. Some of the STAT5 targets identified are upregulated in several human cancers, suggesting that they might represent potential oncogenes in STAT5-associated malignancies."'
GSE10389-GPL82_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"STAT5A and STAT5B proteins belong to the family of signal transducers and activators of transcription. They are encoded by 2 separate genes with 91% identity in their amino acid sequences. Despite their high degree of conservation, STAT5A and STAT5B exert non-redundant functions, resulting at least in part from differences in target gene activation. To better characterize the differential contribution of STAT5A and STAT5B in gene regulation, we performed single or double knock-down of STAT5A and STAT5B using small interfering RNA. Subsequent gene expression profiling and RT-qPCR analyses of IL-3-stimulated Ba/F3-beta cells led to the identification of putative novel STAT5 target genes. Chromatin immunoprecipitation assays analyzing the corresponding gene loci identified unusual STAT5 binding sites compared to conventional STAT5 responsive elements. Some of the STAT5 targets identified are upregulated in several human cancers, suggesting that they might represent potential oncogenes in STAT5-associated malignancies."'
GSE10389-GPL82_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Ba/F3-beta cells transfected with either control (scramble I) or Stat5A and Stat5B siRNAs were stimulated with IL-3 for either 30 minutes or 2 hours.  Unstimulated Ba/F3-beta cells transfected with scramble I siRNA were used as a control. "'
GSE10389-GPL82_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Total RNA was isolated using the RNeasy Maxi kit, including an on-column DNase I treatment to eliminate genomic DNA contamination, according to the manufacturer’s protocol (Qiagen, Valencia, CA). DNase-treated total RNA (5 µg) was synthesized into biotinylated cRNA probe using one-cycle target labeling and IVT labeling (Affymetrix, Inc., Santa Clara, CA) according to manufacturer’s instructions. Fifteen µg of biotinylated cRNA probe from each sample was hybridized onto murine U74A, U74B, U74C Affymetrix Microarray chips. The hybridized chips were then washed using the Affymetrix GeneChip Fluidics 400 station and scanned in the Affymetrix GeneChip Scanner 3000 (Affymetrix, Inc., Santa Clara, CA) according to manufacturer’s instructions.  The quality of cRNA probe synthesis and efficiency of hybridization was analyzed in the GeneChip Operating System for each Affymetrix chip once scanning was complete. Microarray data were normalized using MAS5 and then analyzed using the Genespring (Agilent, Palo Alto, CA). "'
GSE10389-GPL82_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Out of the 36,767 genes, 14,553 passed our noise and P/M/A call filters. Genes were further selected for being stimulated at least 2-fold by IL-3 after 30 minutes (164 genes) and 2 hours (553 genes) stimulation compared to the unstimulated cells (ScI-transfected cells). Then, IL-3 induced genes that were down-regulated at least 2-fold in the STAT5A/B siRNA-transfected cells at 30 minutes and 2 hours (12 and 29 respectively) were identified as putative STAT5 target genes and further investigated. "'
GSE10389-GPL82_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Out of the 36,767 genes, 14,553 passed our noise and P/M/A call filters. Genes were further selected for being stimulated at least 2-fold by IL-3 after 30 minutes (164 genes) and 2 hours (553 genes) stimulation compared to the unstimulated cells (ScI-transfected cells). Then, IL-3 induced genes that were down-regulated at least 2-fold in the STAT5A/B siRNA-transfected cells at 30 minutes and 2 hours (12 and 29 respectively) were identified as putative STAT5 target genes and further investigated. "'
GSE10389-GPL83_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"STAT5A and STAT5B proteins belong to the family of signal transducers and activators of transcription. They are encoded by 2 separate genes with 91% identity in their amino acid sequences. Despite their high degree of conservation, STAT5A and STAT5B exert non-redundant functions, resulting at least in part from differences in target gene activation. To better characterize the differential contribution of STAT5A and STAT5B in gene regulation, we performed single or double knock-down of STAT5A and STAT5B using small interfering RNA. Subsequent gene expression profiling and RT-qPCR analyses of IL-3-stimulated Ba/F3-beta cells led to the identification of putative novel STAT5 target genes. Chromatin immunoprecipitation assays analyzing the corresponding gene loci identified unusual STAT5 binding sites compared to conventional STAT5 responsive elements. Some of the STAT5 targets identified are upregulated in several human cancers, suggesting that they might represent potential oncogenes in STAT5-associated malignancies."'
GSE10389-GPL83_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"STAT5A and STAT5B proteins belong to the family of signal transducers and activators of transcription. They are encoded by 2 separate genes with 91% identity in their amino acid sequences. Despite their high degree of conservation, STAT5A and STAT5B exert non-redundant functions, resulting at least in part from differences in target gene activation. To better characterize the differential contribution of STAT5A and STAT5B in gene regulation, we performed single or double knock-down of STAT5A and STAT5B using small interfering RNA. Subsequent gene expression profiling and RT-qPCR analyses of IL-3-stimulated Ba/F3-beta cells led to the identification of putative novel STAT5 target genes. Chromatin immunoprecipitation assays analyzing the corresponding gene loci identified unusual STAT5 binding sites compared to conventional STAT5 responsive elements. Some of the STAT5 targets identified are upregulated in several human cancers, suggesting that they might represent potential oncogenes in STAT5-associated malignancies."'
GSE10389-GPL83_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Ba/F3-beta cells transfected with either control (scramble I) or Stat5A and Stat5B siRNAs were stimulated with IL-3 for either 30 minutes or 2 hours.  Unstimulated Ba/F3-beta cells transfected with scramble I siRNA were used as a control. "'
GSE10389-GPL83_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Total RNA was isolated using the RNeasy Maxi kit, including an on-column DNase I treatment to eliminate genomic DNA contamination, according to the manufacturer’s protocol (Qiagen, Valencia, CA). DNase-treated total RNA (5 µg) was synthesized into biotinylated cRNA probe using one-cycle target labeling and IVT labeling (Affymetrix, Inc., Santa Clara, CA) according to manufacturer’s instructions. Fifteen µg of biotinylated cRNA probe from each sample was hybridized onto murine U74A, U74B, U74C Affymetrix Microarray chips. The hybridized chips were then washed using the Affymetrix GeneChip Fluidics 400 station and scanned in the Affymetrix GeneChip Scanner 3000 (Affymetrix, Inc., Santa Clara, CA) according to manufacturer’s instructions.  The quality of cRNA probe synthesis and efficiency of hybridization was analyzed in the GeneChip Operating System for each Affymetrix chip once scanning was complete. Microarray data were normalized using MAS5 and then analyzed using the Genespring (Agilent, Palo Alto, CA). "'
GSE10389-GPL83_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Out of the 36,767 genes, 14,553 passed our noise and P/M/A call filters. Genes were further selected for being stimulated at least 2-fold by IL-3 after 30 minutes (164 genes) and 2 hours (553 genes) stimulation compared to the unstimulated cells (ScI-transfected cells). Then, IL-3 induced genes that were down-regulated at least 2-fold in the STAT5A/B siRNA-transfected cells at 30 minutes and 2 hours (12 and 29 respectively) were identified as putative STAT5 target genes and further investigated. "'
GSE10389-GPL83_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Out of the 36,767 genes, 14,553 passed our noise and P/M/A call filters. Genes were further selected for being stimulated at least 2-fold by IL-3 after 30 minutes (164 genes) and 2 hours (553 genes) stimulation compared to the unstimulated cells (ScI-transfected cells). Then, IL-3 induced genes that were down-regulated at least 2-fold in the STAT5A/B siRNA-transfected cells at 30 minutes and 2 hours (12 and 29 respectively) were identified as putative STAT5 target genes and further investigated. "'
GSE10392_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Gene regulation profile of Medroxyprogesterone acetate (MPA)-treated late pregnant cervix"'
GSE10403_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"IL-2 and IL-21 are closely related cytokines that might have arisen by gene duplication. Both cytokines promote the function of effector CD8+ T cells, but their distinct effects on antigen-driven differentiation of naïve CD8+ T cells into effector CD8+ T cells are not clearly understood. We found that antigen-induced expression of eomesodermin and maturation of naïve CD8+ T cells into granzyme B and CD44 expressing effector CD8+ T cells was enhanced by IL-2, but, unexpectedly, suppressed by IL-21. Furthermore, IL-21 repressed expression of IL-2Ra and inhibited IL-2-mediated acquisition of a cytolytic CD8+ T cell phenotype. Despite its inhibitory effects, IL-21 did not induce anergy, but instead potently enhanced the capacity of cells to mediate tumor regression upon adoptive transfer. In contrast, IL-2, surprisingly, impaired the subsequent anti-tumor function of transferred cells. Gene expression studies revealed a distinct IL-21-program that was characterized phenotypically by increased expression of L-selectin and functionally by enhanced anti-tumor immunity that was not reversed by secondary in vitro stimulation with antigen and IL-2. Thus, the efficacy of CD8+ T cells for adoptive immunotherapy can be influenced by opposing differentiation programs conferred by IL-2 and IL-21, a finding with important implications for the development of cellular cancer therapies."'
GSE10403_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"IL-2 and IL-21 are closely related cytokines that might have arisen by gene duplication. Both cytokines promote the function of effector CD8+ T cells, but their distinct effects on antigen-driven differentiation of naïve CD8+ T cells into effector CD8+ T cells are not clearly understood. We found that antigen-induced expression of eomesodermin and maturation of naïve CD8+ T cells into granzyme B and CD44 expressing effector CD8+ T cells was enhanced by IL-2, but, unexpectedly, suppressed by IL-21. Furthermore, IL-21 repressed expression of IL-2Ra and inhibited IL-2-mediated acquisition of a cytolytic CD8+ T cell phenotype. Despite its inhibitory effects, IL-21 did not induce anergy, but instead potently enhanced the capacity of cells to mediate tumor regression upon adoptive transfer. In contrast, IL-2, surprisingly, impaired the subsequent anti-tumor function of transferred cells. Gene expression studies revealed a distinct IL-21-program that was characterized phenotypically by increased expression of L-selectin and functionally by enhanced anti-tumor immunity that was not reversed by secondary in vitro stimulation with antigen and IL-2. Thus, the efficacy of CD8+ T cells for adoptive immunotherapy can be influenced by opposing differentiation programs conferred by IL-2 and IL-21, a finding with important implications for the development of cellular cancer therapies."'
GSE10403_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Keywords: Cytokine exposure comparison"'
GSE10417_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We found that bezafibrate, PPAR-alpha agonist, increased EEG delta oscillation throughout 24 hours and decreased body temperature especially in the later half of the dark period in mice. This DNA- microarray experiment was performed due to investigate the gene expression at ZT10, when body temperature showed no difference between nomal- and bezafibrate-treated mice, and ZT22, when body temperature showed the largest difference between the groups."'
GSE10417_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Both bezafibrate-treated and control mice were decapitated at each ZT10 and ZT22. Total RNA were purified from the hypothalamus of these mice. The one GSM sample of microarray analysis was resulted from equal amount of total RNA mixture of 4 mice in the same condition. Hybridizations were performed using Agilent Whole Mouse Genome oligonucleotide microarray. "'
GSE10421_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Background & Aims: Although hepcidin expression was shown to be induced by the BMP signaling pathway, it is not yet known how iron regulates hepcidin and which of the BMP molecules is the endogenous regulator of iron homeostasis in vivo. We therefore assessed liver transcription profiles of mice fed an iron-deficient or an iron-enriched diet and looked for genes that were regulated similarly to hepcidin in that context."'
GSE10421_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Methods: Genome-wide liver expression profiles of mice of the B6 and D2 genetic backgrounds subjected to iron-deficient, -balanced, or -enriched diets were obtained using Agilent Whole Genome microarrays. Real-time quantitative-PCR and western-blots were used to confirm microarray results and compare gene expression variations induced by secondary iron deficiency or iron overload with those consecutive to Smad4 or Hamp1-deficiency. "'
GSE10421_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Results: Among 1419 transcripts significantly modulated by the dietary iron content, four were regulated similarly to the hepcidin genes Hamp1 and Hamp2. They are coding for Bmp6, the regulator of Bmp/Smad signal transduction Smad7, the negative regulator of basic helix-loop-helix (bHLH) proteins Id1, and a protein with a bHLH domain, Atoh8. The iron overload developed by Smad4 and Hamp1-deficient mice also increased Bmp6 transcription. Body iron stores influence Smad1/5/8 phosphorylation and, as shown by analysis of mice with liver-specific disruption of Smad4, the binding partner for the receptor-activated Smads is necessary for activation of Smad7, Id1, and Atoh8 transcription by iron."'
GSE10422_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Tumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-κB2 (NF-κB2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family).  This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo.  We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling.  As Baff-tg mice display a similar phenotype, and have a genetic modification which acts in the same pathway, yet further up, than TRAF2 and TRAF3, we wished to compare and contrast Baff-tg B cells with TRAF2 and TRAF3 deficient B cells.  This analysis should identify genes that are important in B cell survival."'
GSE10454_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Adult male Swiss Webster mice (30-35 g) were anesthetized, a bipolar electrode was implanted adjacent to the sciatic nerve and the hindlimb immobilized. The voltage-force relation was determined to establish supramaximal stimulation conditions and the length-tension relation was determined to set the resting length for maximum twitch tension. Contractions were induced by sciatic nerve stimulation (0.5 msec duration, 2-5 volts). The muscles were allowed to rest 15 minutes for full metabolic recovery at physiologic temperatures. Supramaximal stimulation was applied at a rate of 10 Hz for 4 hours. At the end of each experiment the extensor digitorum longus (EDL) muscles were carefully dissected and flash frozen in liquid nitrogen for analysis of mRNA expression via microarray analysis. The contralateral, unstimulated EDL provided a genetically matched, paired control for each specimen."'
GSE10454_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study.  An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus.  Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL.  Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE10454_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study.  An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus.  Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL.  Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE10467_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Mammalian microRNAs (miRNAs) are emerging as key regulators of the development and function of the immune system. Here, we report a strong but transient induction of miR-155 in mouse bone marrow after injection of bacterial lipopolysaccharide (LPS) correlated with granulocyte/monocyte (GM) expansion. Demonstrating the sufficiency of miR-155 to drive GM expansion, enforced expression in mouse bone marrow cells caused GM proliferation in a manner reminiscent of LPS treatment. However, the mir-155-induced GM populations displayed pathological features characteristic of myeloid neoplasia. Extending possible relevance to human disease, miR-155 was overexpressed in the bone marrow of patients with acute myeloid leukemia (AML). Furthermore, miR-155 repressed a subset of genes implicated in hematopoietic development and disease. These data implicate miR-155 as a contributor to physiological GM expansion during inflammation and to certain pathological features associated with AML, emphasizing the importance of proper miR-155 regulation in developing myeloid cells during times of inflammatory stress."'
GSE10467_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Construct stable RAW264.7 mouse macrophage cell lines expressing mir-155 or empty vector. RNA is extracted and global gene expression analysis performed to identify mir-155 regulated mRNAs."'
GSE10470_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Oxidative stress is pathogenic in neurological diseases including stroke. The identity of oxidative stress-inducible transcription factors and their role(s) in propagating the death cascade are poorly understood. Microarray analysis of neurons undergoing oxidative stress showed significant induction of prodeath genes. These genes have been shown to be regulated by the bZip transcription factor, ATF4. ATF4 protein localized to the promoter of a putative death gene in neurons in vitro and in vivo. Germline deletion of ATF4 in neurons resulted in a reduction in oxidative stress-induced gene expression and resistance to oxidative death. ATF4 knockout mice experienced significantly smaller infarcts and improved behavioral recovery as compared to wild-type mice subjected to the same reductions in blood flow in a rodent model of stroke. ATF4 modulates an early, upstream event in the death pathway, as resistance to oxidative death by ATF4 deletion was associated with decreased consumption of  the antioxidant glutathione. Restoration of ATF4 protein in knockout neurons was sufficient to restore sensitivity to oxidative death and to reaccelerate loss of glutathione. Together, these findings establish ATF4 as a redox-regulated, pro-death transcriptional activator in the nervous system that propagates death responses to oxidative stress in vitro and to stroke in vivo."'
GSE10478_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"In this study, we performed the gene expression analysis of the Normal, Diabetic and AAT treated NOD mice to elucidate the transcriptional changes induced by AAT. This will assist in identifying the biological processes / pathways involved in curative mechanism of AAT."'
GSE10478_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In this study, we performed the gene expression analysis of the Normal, Diabetic and AAT treated NOD mice to elucidate the transcriptional changes induced by AAT. This will assist in identifying the biological processes / pathways involved in curative mechanism of AAT."'
GSE10478_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Duplicate samples of Normal, Diabetic and AAT treated NOD mice were analyzed."'
GSE10503_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Postnatal day 17 or 28 mice were used for the microarray analysis.  Total RNA was extracted from livers of either Hdac3 wild-type/heterozygous mice expressing Albumin-Cre or Hdac3-null livers, and pooled together in groups of 5.  One pool of control or Hdac3-null liver RNA from both time points was used in technical replicates, meaning each sample was run in duplicate on separate lots of microarray chips to determine reproducibility of the Applied Biosystems ABI1700 chips.  The second set of RNA pools were used as biological replicates for each group at each time point."'
GSE10530_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"Card9 dependent activation of macrophages by TDB"'
GSE10530_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Bone marrow derived macrophages from wt and card9 KO mice were stimulated  with CpG, Curdlan or TDB, an analogon to the mycobacterial cord factor TDM for 48h, respectively."'
GSE10530_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"wt or card9 KO macrophages stimulated for 48h"'
GSE10532_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"Comparison of CpG and TDB induced activation patterns in macrophages."'
GSE10532_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Comparison of CpG and TDB induced activation patterns in macrophages."'
GSE10534_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_title	"Gene expression of mouse ES cells in Gata6 overexpression experiments"'
GSE10534_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_overall_design	"Gata6 overexpression induces differentiation of ES cells."'
GSE10552_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Efficient and sustained knockdown of DNMT1 transcript and protein was achieved using a consecutive transfection protocol in the mouse pituitary adenoma cell line, AtT-20.  Genome wide microarray analysis identified 91 transcripts that were significantly differentially expressed relative to cells treated with a non-targeting control."'
GSE10552_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"AtT-20 cells were repeatedly treated with 20 nM siRNA (siDNMT1 or siNT) over an eight day period.  After eight days total RNA was extracted and prepared for microarray analysis.  The procedure was repeated three times independently."'
GSE10563_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Primary keratinocytes treated with Tamoxifen"'
GSE10563_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Primary keratinocytes were infected with an EMPTY retrovirus and treated with with Tamoxifen, cells were collected every 20 minutes up to 1 hours, and every hour up to 4 hours."'
GSE10594_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Salmonella enterica serotype Typhimurium causes an acute inflammatory reaction in the cecum of streptomycin pre-treated mice. We determined global changes in gene expression elicited by serotype Typhimurium in the cecal mucosa. The gene expression profile was dominated by T cell derived cytokines and genes whose expression is known to be induced by these cytokines. Markedly increased mRNA levels of interferon (IFN-gamma), interleukin-22 (IL-22) and IL-17 were detected by quantitative real-time PCR. Furthermore, mRNA levels of genes whose expression is induced by IFN-gamma, IL-22 or IL-17, including macrophage inflammatory protein 2 (MIP-2), inducible nitric oxide synthase (Nos2), lipocalin-2, MIP-1alpha, MIP-1beta, and keratinocyte-derived cytokine (KC), were also markedly increased. To assess the importance of T cells in orchestrating this pro-inflammatory gene expression profile, we depleted T cells using a monoclonal antibody prior to investigating cecal inflammation caused by serotype Typhimurium in streptomycin pre-treated mice. Depletion of CD3+ T cells resulted in a dramatic reduction in gross pathology, a significantly reduced recruitment of neutrophils and a marked reduction in mRNA levels of IFN-gamma, IL-22, IL-17, iNOS, lipocalin-2 and KC. Our results suggest that T cells play an important role in amplifying inflammatory responses induced by serotype Typhimurium in the cecal mucosa."'
GSE10594_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Salmonella enterica serotype Typhimurium causes an acute inflammatory reaction in the cecum of streptomycin pre-treated mice. We determined global changes in gene expression elicited by serotype Typhimurium in the cecal mucosa. The gene expression profile was dominated by T cell derived cytokines and genes whose expression is known to be induced by these cytokines. Markedly increased mRNA levels of interferon (IFN-gamma), interleukin-22 (IL-22) and IL-17 were detected by quantitative real-time PCR. Furthermore, mRNA levels of genes whose expression is induced by IFN-gamma, IL-22 or IL-17, including macrophage inflammatory protein 2 (MIP-2), inducible nitric oxide synthase (Nos2), lipocalin-2, MIP-1alpha, MIP-1beta, and keratinocyte-derived cytokine (KC), were also markedly increased. To assess the importance of T cells in orchestrating this pro-inflammatory gene expression profile, we depleted T cells using a monoclonal antibody prior to investigating cecal inflammation caused by serotype Typhimurium in streptomycin pre-treated mice. Depletion of CD3+ T cells resulted in a dramatic reduction in gross pathology, a significantly reduced recruitment of neutrophils and a marked reduction in mRNA levels of IFN-gamma, IL-22, IL-17, iNOS, lipocalin-2 and KC. Our results suggest that T cells play an important role in amplifying inflammatory responses induced by serotype Typhimurium in the cecal mucosa."'
GSE10598_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"Transcriptional profile of rapidly stimulated atrial myocytes: Conservation with human atrial fibrillation"'
GSE10598_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Atrial fibrillation (AF) is a progressive arrhythmia for which current therapy is inadequate. During AF, rapid stimulation causes atrial remodeling that promotes further AF. The cellular signals that trigger this process remain poorly understood, however, and elucidation of these factors would likely identify new therapeutic targets. We have previously shown that immortalized mouse atrial (HL-1) myocytes subjected to 24 hr of rapid stimulation in culture undergo remodeling similar to that seen in animal models of atrial tachycardia (AT) and human AF. This preparation is devoid of confounding in vivo variables that can modulate gene expression (e.g., hemodynamics). Therefore, we investigated the transcriptional profile associated with early atrial cell remodeling. RNA was harvested from HL-1 cells cultured for 24 hr in the absence and presence of rapid stimulation and subjected to microarray analysis. Data were normalized using Robust Multichip Analysis (RMA), and genes exhibiting significant differential expression were identified using the Significance Analysis of Microarrays (SAM) method. Using this approach, 919 genes were identified that were significantly altered with rapid stimulation (763 up-regulated and 156 down-regulated). For many individual transcripts, changes typical of AF/AT were observed, with marked up-regulation of genes encoding BNP and ANP precursors, heat shock proteins, and MAP kinases, while novel signaling pathways and molecules were also identified. Both stress and survival response were evident, as well as up-regulation of multiple transcription factors. Genes were also functionally classified based on cellular component, biologic process, and molecular function using the Gene Ontology database to permit direct comparison of our data with other gene sets regulated in human AF and experimental AT. For broad categories of genes grouped by functional classification, there was striking conservation between rapidly stimulated HL-1 cells and AF/AT. Results were confirmed using real-time quantitative RT-PCR on 13 genes selected by physiological relevance in AF/AT and regulation in the microarray analysis (up, down, and nonregulated). Rapidly-stimulated atrial myocytes provide a complementary experimental paradigm to explore the initial cellular signals in AT remodeling to identify novel targets in the treatment of AF."'
GSE10598_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Keywords: stimulated atrial myocytes human atrial fibrillation"'
GSE10626_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Under various pathophysiological muscle-wasting conditions like diabetes and starvation, a family of ubiquitin ligases, including MuRF1 (Muscle specific RING-Finger protein 1), are induced to target muscle proteins for degradation via ubiquitination. In an attempt to identify the in vivo targets of MuRF1 we have generated transgenic mouse lines overexpressing MuRF1 in a skeletal muscle specific fashion. MuRF1-TG lines were viable and had normal fertility. Characterization of their skeletal muscles did not reveal evidence for muscle wasting at 10 weeks of age. In this experiment we compared the skeletal muscle transcriptome of transgenic mice with wildtypes."'
GSE10626_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Under various pathophysiological muscle-wasting conditions like diabetes and starvation, a family of ubiquitin ligases, including MuRF1 (Muscle specific RING-Finger protein 1), are induced to target muscle proteins for degradation via ubiquitination. In an attempt to identify the in vivo targets of MuRF1 we have generated transgenic mouse lines overexpressing MuRF1 in a skeletal muscle specific fashion. MuRF1-TG lines were viable and had normal fertility. Characterization of their skeletal muscles did not reveal evidence for muscle wasting at 10 weeks of age. In this experiment we compared the skeletal muscle transcriptome of transgenic mice with wildtypes."'
GSE10626_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"Keywords: MuRF1 transgene overexpression"'
GSE10627_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Mll-AF9 induced changes in gene expression in various hematopoietic cells"'
GSE10639_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Increased fat intake is associated with obesity and insulin resistance. In some individuals, a failure of pancreatic b-cells to increase insulin production in response to the high demands of obesity leads to diabetes. We sought to determine whether the impaired b- cell adaptation in obesity is associated with differential expression of genes involved in b-cell expansion and intermediary metabolism. Two strains of inbred mice prone to obesity, C57Bl/6J and AKR/J, were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57Bl/6J mice on regular rodent chow or high fat diet. Insulin secretion was 3.2 fold higher in AKR/J than C57Bl/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4 fold greater in AKR/J compared with C57Bl/6J. To elucidate the factors associated with the differences in insulin, we analyzed the gene expression profiles in pancreatic islets in AKR/J and C57Bl/6J mice. Of 14,000 genes examined, 220 were up-regulated and 286 were down-regulated in islets from diet-induced obese AKR/J mice compared with C57Bl/6J mice. Key genes involved in islet signaling and metabolism, e.g. glucagon like peptide-1 receptor, sterol Co-A desaturase 1 & 2 and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function. "'
GSE10639_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Increased fat intake is associated with obesity and insulin resistance. In some individuals, a failure of pancreatic b-cells to increase insulin production in response to the high demands of obesity leads to diabetes. We sought to determine whether the impaired b- cell adaptation in obesity is associated with differential expression of genes involved in b-cell expansion and intermediary metabolism. Two strains of inbred mice prone to obesity, C57Bl/6J and AKR/J, were fed regular rodent chow or high-fat diet, after which islet morphology, secretory function and gene expression were assessed. AKR/J had lower blood glucose and higher insulin levels compared with C57Bl/6J mice on regular rodent chow or high fat diet. Insulin secretion was 3.2 fold higher in AKR/J than C57Bl/6J mice following intraperitoneal glucose injection. Likewise, glucose-stimulated insulin secretion from isolated islets was higher in AKR/J. Additionally, islet mass was 1.4 fold greater in AKR/J compared with C57Bl/6J. To elucidate the factors associated with the differences in insulin, we analyzed the gene expression profiles in pancreatic islets in AKR/J and C57Bl/6J mice. Of 14,000 genes examined, 220 were up-regulated and 286 were down-regulated in islets from diet-induced obese AKR/J mice compared with C57Bl/6J mice. Key genes involved in islet signaling and metabolism, e.g. glucagon like peptide-1 receptor, sterol Co-A desaturase 1 & 2 and fatty acid desaturase 2 were upregulated in obese AKR/J mice. The expression of multiple extracellular matrix proteins was also increased in AKR/J mice, suggesting a role in modulation of islet mass. Functional analyses of differentially regulated genes hold promise for elucidating factors linking obesity to alterations in islet function. "'
GSE10640-GPL4783_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Previous work has demonstrated the potential for peripheral blood (PB) gene expression profiling for the detection of disease or environmental exposures.    We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses."'
GSE10640-GPL4783_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses.  Neither genotype differences nor the time of PB sampling caused any lessening of the accuracy of PB signatures to predict radiation exposure, but sex difference did influence the accuracy of the prediction of radiation exposure at the lowest level (50 cGy).   A PB signature of sepsis was also generated and both the PB signature of radiation and the PB signature of sepsis were found to be 100% specific at distinguishing irradiated from septic animals.  We also identified human PB signatures of radiation exposure and chemotherapy treatment which distinguished irradiated patients and chemotherapy-treated individuals within a heterogeneous population with accuracies of 90% and 81%, respectively."'
GSE10640-GPL4783_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses.  Neither genotype differences nor the time of PB sampling caused any lessening of the accuracy of PB signatures to predict radiation exposure, but sex difference did influence the accuracy of the prediction of radiation exposure at the lowest level (50 cGy).   A PB signature of sepsis was also generated and both the PB signature of radiation and the PB signature of sepsis were found to be 100% specific at distinguishing irradiated from septic animals.  We also identified human PB signatures of radiation exposure and chemotherapy treatment which distinguished irradiated patients and chemotherapy-treated individuals within a heterogeneous population with accuracies of 90% and 81%, respectively."'
GSE10640-GPL6524_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Previous work has demonstrated the potential for peripheral blood (PB) gene expression profiling for the detection of disease or environmental exposures.    We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses."'
GSE10640-GPL6524_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses.  Neither genotype differences nor the time of PB sampling caused any lessening of the accuracy of PB signatures to predict radiation exposure, but sex difference did influence the accuracy of the prediction of radiation exposure at the lowest level (50 cGy).   A PB signature of sepsis was also generated and both the PB signature of radiation and the PB signature of sepsis were found to be 100% specific at distinguishing irradiated from septic animals.  We also identified human PB signatures of radiation exposure and chemotherapy treatment which distinguished irradiated patients and chemotherapy-treated individuals within a heterogeneous population with accuracies of 90% and 81%, respectively."'
GSE10640-GPL6524_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses.  Neither genotype differences nor the time of PB sampling caused any lessening of the accuracy of PB signatures to predict radiation exposure, but sex difference did influence the accuracy of the prediction of radiation exposure at the lowest level (50 cGy).   A PB signature of sepsis was also generated and both the PB signature of radiation and the PB signature of sepsis were found to be 100% specific at distinguishing irradiated from septic animals.  We also identified human PB signatures of radiation exposure and chemotherapy treatment which distinguished irradiated patients and chemotherapy-treated individuals within a heterogeneous population with accuracies of 90% and 81%, respectively."'
GSE10644_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mice were maintained for 2 weeks on a 12 hour light/dark (LD) cycle (lights on 7 AM, lights off 7 PM) prior to all experiments. For the reference experiment, mice had ad libitum access to food. Samples were collected every four hours, at 0400, 0800, 1200, 1600, 2000 and 2400, starting 1 hour after the lights went on.  Total RNA was isolated by modified guanidinium thicyanate-phenol-chloroform extraction method and was treated with DNase I (Promega, Madison, WI) at 37 oC for 30 minutes.Hybridizations and Scaning were done as per Affymetrix techniques. Three MOE 430 plus 2.0 chips were used per time point."'
GSE10651_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	" Using a TCR transgenic transplantation model a series of differently modulated bmDC (IL10, TGFb and VD3 treated, +/-LPS) were established that could mediate tolerance following adaptive transfer.  These modified cells, in contrast to untreated 'immature' bmDC retained their capacity to tolerise following exposure to LPS.  The unmodified, non-tolerogenic, LPS-treated cells provided a comparator population to facilitate investigation into molecular expression patterns that correlate with functional phenotype."'
GSE10651_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	" Using a TCR transgenic transplantation model a series of differently modulated bmDC (IL10, TGFb and VD3 treated, +/-LPS) were established that could mediate tolerance following adaptive transfer.  These modified cells, in contrast to untreated 'immature' bmDC retained their capacity to tolerise following exposure to LPS.  The unmodified, non-tolerogenic, LPS-treated cells provided a comparator population to facilitate investigation into molecular expression patterns that correlate with functional phenotype."'
GSE10652_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Keywords: treated vs non treated"'
GSE10654_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Hepatic ischemia/reperfusion (I/R) injury is a complication of liver surgery, transplantation and shock.  Our previous studies have suggested there is an age-dependent response to I/R.  In the present study, we examined global gene expression after liver I/R in young (4-5 weeks) and adult (12-14 months) mice using Affymetrix microarray.  Gene expression was filtered based on a change in expression of 1.5-fold relative to respective controls and then analyzed by ANOVA.  Seventy-two genes in young mice and 56 genes in adult mice had significantly increased expression.  Of these, only 18 were up-regulated in both age groups.  In young mice, 289 genes were down-regulated whereas in adult mice, 874 genes were decreased.  Of these genes, 175 genes were decreased in both groups.  Pathway and network analyses of up- and down-regulated gene lists revealed a number of notable differences between young and adult mice.  Of these, we found that genes related to the activating protein-1 (AP-1) pathway were upregulated preferentially in young mice.  This corresponded with an increase in AP-1 activation in young versus adult mice.  Finally, we found that genes related to the ubiquitin-proteasome pathway were selectively down-regulated in adult mice.  This was accompanied by reduced degradation of the inhibitory protein, I?B?, in adult mice.  The data demonstrate specific, pathway- and network-related differences in gene expression profiles between young and adult mice in the response to I/R.  More specifically, we have identified two pathways that may contribute to the superior response to I/R in young mice which represent potential therapeutic targets."'
GSE10654_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Keywords: treated vs non treated"'
GSE10659_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"6 samples RFC KO mouse embryos, E9.5, folic acid treated: 3 Control, Wildtype, normal; 3 Affected, Nullizygous, CR/chorioallantoic defect; as paired-littermates with one normal and one affected embryo per set from each of three separate litters for RNA extraction and hybridization on Affymetrix microarrays."'
GSE10666_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The stability, localization and translation of mammalian mRNAs are largely determined by sequences in the 3' untranslated region (UTR).  Here, we describe a conserved program of increased upstream polyadenylation site usage following activation of primary murine CD4+ T lymphocytes.  This program, resulting in shorter 3' UTRs, is a characteristic of immune cell activation and strongly correlates with proliferation across diverse cell types and tissues.  Enforced expression of full-length 3' UTRs confers differences in protein expression that can in some cases be eliminated by deletion of predicted microRNA target sites in the variably included region. Together, our data indicate that polyadenylation site usage is coordinately regulated such that states of increased proliferation are associated with widespread reduction of 3' UTR-based regulation."'
GSE10666_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Keywords: activation, exon array, time course"'
GSE10678_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Dysfunction of the dystrophin-glycoprotein complex (DGC) is a frequent cause of hereditary forms of muscular dystrophy. Although DGC function in maintaining skeletal muscle integrity has been well characterized, little is known about how the DGC complex is coordinately regulated at the transcriptional level.  To test this hypothesis, we engineered HDAC4 stably overexpressing and control myotubes in an in vitro model of muscle differentiation.  Here we present evidence that HDAC4, a neural activity-responsive histone deacetylase, is a critical transcriptional regulator of the DGC complex. We show that HDAC4 can repress multiple components of the DGC complex, including dystrophin and sarcoglycan family members in both cultured myotubes.  To confirm this finding, the protein levels of core DGC complex members including dystrophin, sarcoglycan complex members, and additional dystrophin-associated proteins were evaluated in differentiated myotubes by western analysis. "'
GSE10678_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"C2C12 mouse myotubes were infected with either a HDAC4 expressing or control (Neo) retroviruses.  After stable selection, myotubes were differentiated at 90% confluency in 2% horse serum (Hyclone) for 4 days.  At this time point, RNA was extracted and the two types of cells compared in a microarray analysis.   "'
GSE10682_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Gene Expression analysis was carried out using the Affymetrix Mouse 430 A 2.0 chips representing about 22,629 full-length genes and ESTs.  Initial scaling was done using the Affymetrix  Microarray Suite Expression Software version 5.0 and subsequent analysis was done using GeneSpring Software version 6.1 ( Silicon Genetics).     (Tumor derived cell lines) /in vivo selected cell lines were compared to the parental cell lines from which they were derived.  We had two parental cell  line samples which were defined as replicates and treated as a single sample and 4 cell lines namely TD A, B, C and D derived from the parents.      Three different filtering conditions were applied.  First, we applied Expression Percentage Restriction retaining only those genes  which had a raw expression value of 80.0 or more in at least 1 out of the 5 samples being compared.  This enabled us to filter out the low-intensity values while retaining genes that may have a very low expression level in one sample but may be switched on in another sample.  The cut-off value of 80.00 was determined by analyzing the raw data of each of the chips being compared and estimating the average background expression value.  Of the 22,629 genes represented on the chips, 11,418 genes were retained.    Secondly, we filtered on data quality selecting for genes with a Flag value of Present (P) in all the samples being compared.  10,126 genes were retained after applying this filter.    We then carried out a pair-wise fold-change analysis comparing each tumor derived cell line to the parental cell-line.  We retained genes that underwent at least 2 folds or more up-regulation or down-regulation in the tumor derived cell l  ines, compared to the parentals.  1,010 genes were retained after this step.    In order to identify genes that underwent statistically significant changes in gene expression in the tumor derived cell-lines when compared to the parentals we applied a statistical filter analysis and performed the Student’s-t-test with a p value cut-off of 0.05.  Multiple testing correction was turned off.  We found 123 genes that were over-expressed and 5 that were underexpressed.    We carried out two-way hierarchical clustering using the GeneSpring Software 6.1 using standard correlation as similarity metric.  We also analyzed our data using Venn Diagrams in order to identify the statistically significant genes that were common to all 4 tumor derived cell-lines. We obtained 55 that were up-regulated while there were 5 which were down-regulated and common to all four cell-lines."'
GSE10684_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have anti-oxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Mdr1a-/- mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. This study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0.2% curcumin or control + 0.1% rutin and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways probably mediated by PXR and PPARalpha activation of RXR. These results reveal the potential of global gene expression and pathway analyses to study and better understand the effect of foods in colonic inflammation."'
GSE10702_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The in vivo properties of HR-HPV E6 and E7 oncoproteins have been previously evaluated through the generation and characterization of HPV transgenic mouse strains. Although K14E6 transgenic mice develop spontaneous tumors of the skin epithelium, no spontaneous reproductive tract malignancies arise, unless the transgenic mice were treated chronically with 17β-estradiol. Taken together, these findings suggest that E6 performs critical functions in normal adult cervix and skin, highlighting the need to define E6-controlled transcriptional programs in these tissues. We evaluated the different expression profile of 14,000 genes in skin or cervix from young K14E6 transgenic mice compared with corresponding tissues from non-transgenic (FVB) mice."'
GSE10741_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Toll-like Receptor 3-induced Suppression via Binding of Suppressors of Cytokine Signaling 3 to Tyrosine Kinase 2"'
GSE10741_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The Suppressor of cytokine signaling (SOCS) family of negative regulatory proteins are upregulated in response to several cytokines and pathogen-associated molecular patterns (PAMPs), and suppress cellular signaling responses by binding receptor phosphotyrosine residues. Exposure of bone marrow-derived dendritic cells (BMDCs) to 1D8 cells, a murine model of ovarian carcinoma, suppresses their ability to express CD40 and stimulate antigen specific responses in response to PAMPs, and in particular to poly I: C with the upregulated SOCS3 transcript and protein levels. The ectopic expression of SOCS3 in both the macrophage cell line RAW264.7 and BMDCs decreased signaling in response to both poly I:C and IFNα. Further, knockdown of SOCS3 transcripts significantly enhanced the responses of RAW264.7 and BMDCs to both poly I: C and IFNα. Immunoprecipitation and pull-down studies demonstrate that SOCS3 binds to the IFNα receptor TYK2. Since poly I: C triggers autocrine IFNα signaling, binding of SOCS3 to TYK2 may thereby suppress the activation of BMDCs by polyI:C and IFNα. Thus, elevated levels of SOCS3 in tumor-associated DCs may potentially resist the signals induced by TLR3 ligands and type I interferon to decrease DC activation via binding with IFNα receptor TyK2."'
GSE10741_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The Suppressor of cytokine signaling (SOCS) family of negative regulatory proteins are upregulated in response to several cytokines and pathogen-associated molecular patterns (PAMPs), and suppress cellular signaling responses by binding receptor phosphotyrosine residues. Exposure of bone marrow-derived dendritic cells (BMDCs) to 1D8 cells, a murine model of ovarian carcinoma, suppresses their ability to express CD40 and stimulate antigen specific responses in response to PAMPs, and in particular to poly I: C with the upregulated SOCS3 transcript and protein levels. The ectopic expression of SOCS3 in both the macrophage cell line RAW264.7 and BMDCs decreased signaling in response to both poly I:C and IFNα. Further, knockdown of SOCS3 transcripts significantly enhanced the responses of RAW264.7 and BMDCs to both poly I: C and IFNα. Immunoprecipitation and pull-down studies demonstrate that SOCS3 binds to the IFNα receptor TYK2. Since poly I: C triggers autocrine IFNα signaling, binding of SOCS3 to TYK2 may thereby suppress the activation of BMDCs by polyI:C and IFNα. Thus, elevated levels of SOCS3 in tumor-associated DCs may potentially resist the signals induced by TLR3 ligands and type I interferon to decrease DC activation via binding with IFNα receptor TyK2."'
GSE10741_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Keywords: Response to intracellular signaling from tumor cells by coculture or treated medium"'
GSE10743_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The RET/PTC3 (RP3) fusion gene is the most frequent mutation found in radiation-induced papillary thyroid cancers (PTC). Several studies suggest that the RET/PTC rearrangement is an initiating event in tumorigenesis. E7 is an oncoprotein derived from the Human Papilllomavirus 16 (HPV16) responsible for most cervical carcinoma in women. We studied here the sequence of events leading to thyroid cancer in Tg-RP3 and Tg-E7 mice expressing the transgene exclusively in the thyroid under the control of thyroglobulin (Tg) promoter. Both transgenic mice develop thyroid hyperplasia followed by solid differentiated carcinoma in older animals. To understand the different steps leading to carcinoma, we analyzed thyroid gene expression in both strains at different ages (2, 6, 10 months) by microarray technology. Important biological processes were differentially regulated in the two tumor types. In E7 thyroids cell cycle was the most upregulated process; observation consistent with the huge size of these tumors. In RP3 thyroids immunity was the most significantly regulated process, as previously observed in microarray data on human PTC. Interestingly, other human PTC characteristics were also observed in RP3 but not in E7 mouse tumors: similar regulation of several human PTC markers, upregulation of many EGF-like growth factors and finally significant regulation of angiogenesis and extracellular matrix remodeling-related genes. In summary we showed that RP3 contrary to E7 mouse tumors share several important genotypic characteristics with human PTC, observation reinforcing the validity of this model to study human thyroid tumorigenesis.  "'
GSE10743_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"The RET/PTC3 (RP3) fusion gene is the most frequent mutation found in radiation-induced papillary thyroid cancers (PTC). Several studies suggest that the RET/PTC rearrangement is an initiating event in tumorigenesis. E7 is an oncoprotein derived from the Human Papilllomavirus 16 (HPV16) responsible for most cervical carcinoma in women. We studied here the sequence of events leading to thyroid cancer in Tg-RP3 and Tg-E7 mice expressing the transgene exclusively in the thyroid under the control of thyroglobulin (Tg) promoter. Both transgenic mice develop thyroid hyperplasia followed by solid differentiated carcinoma in older animals. To understand the different steps leading to carcinoma, we analyzed thyroid gene expression in both strains at different ages (2, 6, 10 months) by microarray technology. Important biological processes were differentially regulated in the two tumor types. In E7 thyroids cell cycle was the most upregulated process; observation consistent with the huge size of these tumors. In RP3 thyroids immunity was the most significantly regulated process, as previously observed in microarray data on human PTC. Interestingly, other human PTC characteristics were also observed in RP3 but not in E7 mouse tumors: similar regulation of several human PTC markers, upregulation of many EGF-like growth factors and finally significant regulation of angiogenesis and extracellular matrix remodeling-related genes. In summary we showed that RP3 contrary to E7 mouse tumors share several important genotypic characteristics with human PTC, observation reinforcing the validity of this model to study human thyroid tumorigenesis.  "'
GSE10745_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Methodology/Principal Findings: By chromatin immunoprecipitation, we detected the same heterochromatin marks in homozygous mice carrying a (GAA)230 repeat in the first intron of the mouse frataxin gene (KIKI mice). These animals have decreased frataxin levels and, by microarray analysis, show significant gene expression changes in several tissues. We treated KIKI mice with a novel histone deacetylase inhibitor, compound 106, which substantially increases frataxin mRNA levels in cells from Friedreich ataxia individuals. Treatment increased histone H3 and H4 acetylation in chromatin near the GAA repeat and restored wild-type frataxin levels in the nervous system and heart, as determined by quantitative RT-PCR and semiquantitative western blot analysis. No toxicity was observed. Furthermore, most of the differentially expressed genes in KIKI mice reverted towards wild-type levels. "'
GSE10745_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Two mouse strains (KIKI and KO) were treated with compound 106 or control. Three tissues (Brain, Cerebellum, Heart) were examined in quadruplicate, for a total 48 arrays. "'
GSE10765_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice"'
GSE10765_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Peritoneal macrophages from wild-type, IRAK-2-/- and IRAK-1/IRAK-2 mice were stimulated with MALP-2 for 0, 2, 4, and 8 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."'
GSE10768_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Ciguatoxins (CTX) are polyether neurotoxins responsible for ciguatera, the most common fish-borne food poisoning in humans.  This study characterizes the global transcriptional response of mouse liver to a symptomatic dose (0.26 ng/g) of the highly potent Pacific ciguatoxin-1 (P-CTX-1).  At 1 h post exposure 2.4% of features on a 44K whole genome array were differentially expressed (p ≤ 0.0001), increasing to 5.2% at 4 h and decreasing to 1.4% by 24 h post-CTX exposure.  Early gene expression was likely influenced prominently by an acute 4 °C decline in core body temperature by 1 h, which resolved by 8 h following exposure.  Cytochrome P450s were of particular interest due to their role in xenobiotic metabolism.  Twenty-seven genes, mostly members of Cyp2 and Cyp4 families, showed significant changes in expression.  Many Cyps underwent an initial down-regulation at 1 h but were quickly and strongly up-regulated at 4 and 24 h post exposure.  In addition to Cyps, increases in several glutathione S-transferases were observed, an indication that both phase I and phase II metabolic reactions are involved in the hepatic response to CTX in mice."'
GSE10769_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Mouse and rat models are mainstays in pharmacology, toxicology and drug development – but differences between strains and between species complicate data interpretation and application to human health. Dioxin-like polyhalogenated aromatic hydrocarbons represent a major class of environmentally and economically relevant toxicants. In mammals dioxin exposure leads to a broad spectrum of adverse affects, including hepatotoxicity of varying severity. Several studies have shown that dioxins extensively alter hepatic mRNA levels. Surprisingly, though, analysis of a limited portion of the transcriptome revealed that rat and mouse responses diverge greatly (Boverhof et al. Toxicol Sci 94:398–416, 2006)."'
GSE10769_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Wild-type C57BL/6 mice were treated with 1000 ug/kg TCDD (n=6) or with cornoil vehicle as control (n=5) for 19 hours. Their livers were then excised, RNA extracted, and the resulting samples hybridized to Affymetrix MOE430-2 arrays to survey changes in the transcriptome profile."'
GSE10776_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"Five embryonic stem (ES) cell lines were derived from two F1 hybrid strains that were produced by mating female C57BL6 mice with male DBA2 or CBA/Ca mice. Two-week-old prepubertal female was used for follicle retrieval. All procedures for animal management, breeding, and surgery followed the standard protocols of Seoul National University, Korea. The Institutional Animal Care and Use Committee Review Board at Seoul National University approved our research proposal in April 2005 (approval number: SNU0050331-02). Three parthonogenetic ES embryo cell lines were established from parthenogenetic activation on naturally ovulated oocytes (OpB6D2-SNU-1) and in vitro-growth oocytes (FpB6CBA-SNU8 and FpB6D2-SNU2). Two normal ES embryo cell lines were derived from mating naturally ovulated female mice in estrus with male mice (NmB6D2-SNU-1) and purchased from ATCC. Detailed procedures, including establishment of ES cell lines can be found elsewhere (FpB6CBA-SNU8, FpB6D2-SNU2 and OpB6D2-SNU-1 for and NmB6D2-SNU-1 and OP1 for manuscript in preparation)."'
GSE10796_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"During development of the mammalian central nervous system (CNS), neurons and glial cells (astrocytes and oligodendrocytes) are generated from common neural precursor cells (NPCs). However, neurogenesis precedes gliogenesis, which normally commences at later stages of fetal telencephalic development. Astrocyte differentiation of mouse NPCs at embryonic day (E) 14.5 (relatively late gestation) is induced by activation of the transcription factor STAT3, whereas at E11.5 (mid-gestation) NPCs do not differentiate into astrocytes even when stimulated by STAT3-activating cytokines such as leukemia inhibitory factor (LIF). This can be explained in part by the fact that astrocyte-specific gene promoters are highly methylated in NPCs at E11.5, but other mechanisms are also likely to play a role. We therefore sought to identify genes involved in the inhibition of astrocyte differentiation of NPCs at midgestation. We first examined gene expression profiles in E11.5 and E14.5 NPCs, using Affymetrix GeneChip analysis, applying the Percellome method to normalize gene expression level. We then conducted in situ hybridization analysis for selected genes found to be highly expressed in NPCs at midgestation. Among these genes, we found that N-myc and high mobility group AT-hook 2 (Hmga2) were highly expressed in the E11.5 but not the E14.5 ventricular zone of mouse brain, where NPCs reside. Transduction of N-myc and Hmga2 by retroviruses into E14.5 NPCs, which normally differentiate into astrocytes in response to LIF, resulted in suppression of astrocyte differentiation. However, sustained expression of N-myc and Hmga2 in E11.5 NPCs failed to maintain the hypermethylated status of an astrocyte-specific gene promoter. Taken together, our data suggest that astrocyte differentiation of NPCs is regulated not only by DNA methylation but also by genes whose expression is controlled spatio-temporally during brain development."'
GSE10796_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"During development of the mammalian central nervous system (CNS), neurons and glial cells (astrocytes and oligodendrocytes) are generated from common neural precursor cells (NPCs). However, neurogenesis precedes gliogenesis, which normally commences at later stages of fetal telencephalic development. Astrocyte differentiation of mouse NPCs at embryonic day (E) 14.5 (relatively late gestation) is induced by activation of the transcription factor STAT3, whereas at E11.5 (mid-gestation) NPCs do not differentiate into astrocytes even when stimulated by STAT3-activating cytokines such as leukemia inhibitory factor (LIF). This can be explained in part by the fact that astrocyte-specific gene promoters are highly methylated in NPCs at E11.5, but other mechanisms are also likely to play a role. We therefore sought to identify genes involved in the inhibition of astrocyte differentiation of NPCs at midgestation. We first examined gene expression profiles in E11.5 and E14.5 NPCs, using Affymetrix GeneChip analysis, applying the Percellome method to normalize gene expression level. We then conducted in situ hybridization analysis for selected genes found to be highly expressed in NPCs at midgestation. Among these genes, we found that N-myc and high mobility group AT-hook 2 (Hmga2) were highly expressed in the E11.5 but not the E14.5 ventricular zone of mouse brain, where NPCs reside. Transduction of N-myc and Hmga2 by retroviruses into E14.5 NPCs, which normally differentiate into astrocytes in response to LIF, resulted in suppression of astrocyte differentiation. However, sustained expression of N-myc and Hmga2 in E11.5 NPCs failed to maintain the hypermethylated status of an astrocyte-specific gene promoter. Taken together, our data suggest that astrocyte differentiation of NPCs is regulated not only by DNA methylation but also by genes whose expression is controlled spatio-temporally during brain development."'
GSE10796_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"During development of the mammalian central nervous system (CNS), neurons and glial cells (astrocytes and oligodendrocytes) are generated from common neural precursor cells (NPCs). However, neurogenesis precedes gliogenesis, which normally commences at later stages of fetal telencephalic development. Astrocyte differentiation of mouse NPCs at embryonic day (E) 14.5 (relatively late gestation) is induced by activation of the transcription factor STAT3, whereas at E11.5 (mid-gestation) NPCs do not differentiate into astrocytes even when stimulated by STAT3-activating cytokines such as leukemia inhibitory factor (LIF). This can be explained in part by the fact that astrocyte-specific gene promoters are highly methylated in NPCs at E11.5, but other mechanisms are also likely to play a role. We therefore sought to identify genes involved in the inhibition of astrocyte differentiation of NPCs at midgestation. We first examined gene expression profiles in E11.5 and E14.5 NPCs, using Affymetrix GeneChip analysis, applying the Percellome method to normalize gene expression level. We then conducted in situ hybridization analysis for selected genes found to be highly expressed in NPCs at midgestation. Among these genes, we found that N-myc and high mobility group AT-hook 2 (Hmga2) were highly expressed in the E11.5 but not the E14.5 ventricular zone of mouse brain, where NPCs reside. Transduction of N-myc and Hmga2 by retroviruses into E14.5 NPCs, which normally differentiate into astrocytes in response to LIF, resulted in suppression of astrocyte differentiation. However, sustained expression of N-myc and Hmga2 in E11.5 NPCs failed to maintain the hypermethylated status of an astrocyte-specific gene promoter. Taken together, our data suggest that astrocyte differentiation of NPCs is regulated not only by DNA methylation but also by genes whose expression is controlled spatio-temporally during brain development."'
GSE10806_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Pluripotent stem cells induced from adult neural stem cells by reprogramming with two factors"'
GSE10806_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Reprogramming of somatic cells is a valuable tool to understand the mechanisms of regaining pluripotency and further opens up the possibility of generating patient-specific pluripotent stem cells. Reprogramming of mouse and human somatic cells into pluripotent stem cells, designated as induced pluripotent stem (iPS) cells, has been possible with the expression of the transcription factor quartet Oct4 (also known as Pou5f1), Sox2, c-Myc, and Klf4. Considering that ectopic expression of c-Myc causes tumourigenicity in offspring and retroviruses themselves can cause insertional mutagenesis, the generation of iPS cells with a minimal number of factors may hasten the clinical application of this approach. Here, we show that adult mouse neural stem cells express higher endogenous levels of Sox2 and c-Myc than embryonic stem cells, and that exogenous Oct4 together with either Klf4 or c-Myc are sufficient to generate iPS cells from neural stem cells. These two-factor (2F) iPS cells are similar to embryonic stem cells at the molecular level, contribute to development of the germ line, and form chimeras. We propose that, in inducing pluripotency, the number of reprogramming factors can be reduced when using somatic cells that endogenously express appropriate levels of complementing factors."'
GSE10813_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"To identify candidate genes that might be related to the suppressive activity, the CD8+ NKT cells with potent suppressive activity were compared to three different control cells: 1) CD4+ T cells (with very weak suppression) cultured under the same condition as a control for culture condition, 2) naïve CD8 T cells as the baseline expression level, and 3) CD8+ T cells activated using conventional activation protocols.  The last two cell populations do not possess suppressive activity.  This data set allows us to examine a number of different questions"'
GSE10815_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The mechanisms by which dendritic cells (DCs) induce differentiation of naïve CD4+ T cells  along the Th2 lineage is not well understood given that DCs themselves do not produce IL-4. In the present study, we undertook a microarray approach to identify genes involved in the induction of Th2 differentiation by DCs treated with a Th2-skewing adjuvant cholera toxin (CT). In the microarray analysis, murine bone marrow derived immature DCs were treated with CT. Of particular interest was tthe significant upregulation of the expression of c-kit. The upregulation of c-kit on DCs is critical for the induction of a Th2 response."'
GSE10815_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Murine bone marrow cells were cultured in the presence of GM-CSF (10 ng/ml)  for 6 days . On day 6 the cells were harvested and purified  using magnetically labeled anti mouse CD11c+ beads .  The DCs were stimulated with CT (1 ug/ml)  for 24 hours and the RNA was isolated."'
GSE10817_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"MLL5 is a novel trithorax group gene and a candidate tumor suppressor gene located within a 2.5 Mb interval of chromosome band 7q22 that is frequently deleted in human myeloid malignancy.  Here we show that Mll5 is required for normal hematopoietic stem cell (HSC) homeostasis. Inactivation of the Mll5 gene in mice results in reduced cellularity of the long-term HSC compartment, which correlates with functional impairment of long-term repopulation potential under competitive conditions.  Bone marrow cells from Mll5-deficient mice were defective in spleen colony-forming assays, and the mutant mice showed enhanced susceptibility to 5-Fluorouracil-induced myelosuppression.  Heterozygous and homozygous Mll5 mutant mice did not spontaneously develop hematologic cancers, and loss of Mll5 did not alter the phenotype of a fatal myeloprolferative disorder induced by oncogenic Kras in vivo.  Collectively, the data reveal an important role for Mll5 in HSC homeostasis, and provide a basis for further studies to explore its role in leukemogenesis."'
GSE10823-GPL81_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"TCE is a non-genotoxic hepatocarcinogen in mouse, but not in rat or human. Extrapolation of data from laboratory animals to humans is difficult due to species-specific differences. To identify molecular pathways and biological changes responsible for species-specific differences in hepatocarcinogenesis, we analyzed gene expression profiles of livers from B6C3F1 mice and SD rats administered TCE by oral gavage once or repeatedly every 24 hrs for 14 days. Gene expression analysis revealed distinct clusters of transcriptional profiles in single- and repeated-dose mice and rats.  Pathway analysis showed differences in biological pathways between single- and repeated-dose mice and rats. Activation of the MAPK signaling cascade and ubiquitin-proteasome inhibitory function, as well as inhibition of TGF-beta signaling, were specific to mice and suggest a role in hepatocyte proliferation. Although pathological analysis showed no evidence of apoptosis, gene expression analysis revealed changes in apoptosis-related genes. In addition to the previously reported suppression of apoptosis, results in repeated-dose mice showed that toxicity induced by TCE in turn induces apoptosis."'
GSE10858_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"This analysis compares the signal of DNA from T-cell lymphoblastic lymphomas induced by gamma-irradiation versus normal thymuses"'
GSE10859_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Expression patterns of cDNAs in gamma-irradiation induced T-cell lymphomas"'
GSE10859_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"This set of data contains the expression levels of cDNAs in T-cell lymphoblastci lymphomas induced by gamma-irradiation. These tumor samples were compared to normal thymuses"'
GSE10861-GPL6592_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"T-cell lymphoblastic lymphomas induced by gamma-irradiation"'
GSE10861-GPL6593_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"T-cell lymphoblastic lymphomas induced by gamma-irradiation"'
GSE10861-GPL6606_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"T-cell lymphoblastic lymphomas induced by gamma-irradiation"'
GSE10869_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Effects of CaMKIV loss on cocaine-induced gene expression in the striatum"'
GSE10869_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Our goal was to analyze how loss of CaMKIV will affect acitivity-regulated transcription induced by strong stimulation, i.e. cocaine."'
GSE10870_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Our goal was to analyze how loss of SRF will affect acitivity-regulated transcription induced by strong stimulation, i.e. cocaine."'
GSE10871_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Expression profiles generated during dissection of the molecular mechanisms underlying direct reprogramming of somatic cells to a pluripotent state (induced pluripotent stem cells, iPS). "'
GSE10891_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Gamma-irradiation induced T-cell lymphomas (miRNA study)"'
GSE10891_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"This set of data contains the expression levels of cDNAs in T-cell lymphoblastic lymphomas induced by gamma-irradiation. These tumor samples were compared to normal thymuses"'
GSE10895_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Study on gene expression in multifunctional protein 2 deficient mice. Liver samples of two days old mice in normal conditions are used. In total 8 arrays were hybridized corresponding to 4 KO mice and 4 WT mice Results: Cholesterol synthesis is induced and ppar alpha targets also differentially expressed between KO and WT."'
GSE10900_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"c3h10t1/2 cells were treated with vehicle or 1uM dexamethasone for 90 minutes (3 biological replicates of each)"'
GSE10900_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"hybridized all samples to a pool of RNA from vehicle and treated c3h10t1/2 cells"'
GSE10902_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The LIM-only protein FHL2 acts as a transcriptional modulator that positively or negatively regulates multiple signaling pathways. We recently reported that FHL2 cooperates with CBP/p300 in the activation of ß-catenin/TCF target gene cyclin D1. In this paper, we demonstrate that FHL2 is associated with the cyclin D1 promoter at the TCF/CRE site, providing evidence that cyclin D1 is a direct target of FHL2. We show that deficiency of FHL2 greatly reduces the proliferative capacity of spontaneously immortalized mouse fibroblasts which is associated with decreased expression of cyclin D1 and p16INK4a, and hypophosphorylation of Rb. Reexpression of FHL2 in FHL2-null fibroblasts efficiently restores cyclin D1 levels and cell proliferative capacity, indicating that FHL2 is critical for cyclin D1 activation and cell growth. Moreover, ectopic cyclin D1 expression is sufficient to override growth inhibition of immortalized FHL2-null fibroblasts. Gene expression profiling revealed that FHL2 deficiency triggers a broad change of the cell cycle program that is associated with downregulation of several G1/S and G2/M cyclins, E2F transcription factors and DNA replication machinery, thus correlating with reduced cell proliferation. This change also involves downregulation of the negative cell cycle regulators, particularly INK4 inhibitors, which could counteract the decreased expression of cyclins, allowing cells to grow. Our study illustrates that FHL2 can act on different aspects of the cell cycle program to finely regulate cell proliferation."'
GSE10908_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"Differential gene expression in ADAM10 over-expressing transgenic mice"'
GSE10908_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"To assess the influence of ADAM10 on the gene expression profile in the brain we performed microarray analysis using RNA isolated from brains of five month old mice over-expressing either the α-secretase ADAM10 or a dominant-negative mutant (dn) of this enzyme. As compared to non-transgenic wild-type mice, 355 genes were found to be differentially expressed in ADAM10 transgenic mice and 143 genes in dnADAM10 mice. A higher number of genes was found to be differentially regulated in double-transgenic mouse strains additionally expressing the human APP V717I mutant (APP[V717I]). Thus, α-secretase cleavage of over-expressed APP[V717I] alters CNS gene expression additionally."'
GSE10909_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Murine bone marrow cells were transduced with a retrovirus (MSCV-IRES-GFP, MIG) expressing either NUP98/HHEX or NUP98/HOXA9  (or the empty vector), mRNA was isolated after 72h. Each experiment was performed in triplicates."'
GSE10912_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"Gene expression profiling in BCR/ABL expressing HSCs"'
GSE10912_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"The BCR-ABL oncogene,  generated by Philadelphia chromosome, is present in about 95% human Chronic myeloid leukemia (CML) and 20~30% acute lymphoblastic leukemia (ALL). One of BCR-ABL isoforms, P210, is more often detected in CML and ALL patients. Although BCR-ABL kinase inhibitors are effective in controlling the diseases, they do not provide cure due to the development of drug resistance and the insensitivity of leukemia stem cells to these drugs. Identification of new therapeutic targets is critical. To identify potential target against leukemia stem cells, we studied gene expression in leukemia stem cells, which were identified in mice in our lab (Hu Y, Swerdlow S, Duffy TM, Weinmann R, Lee FY, Li S.  2006. Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia. Proc Natl Acad Sci USA 103(45):16870-16875.). The sorted leukemia stem cells that expressed BCR-ABL were used for isolation of RNA, followed by the analysis of gene expression using the DNA microarray.  The same lineage of non-BCR-ABL-expressing normal hematopoietic stem cells was used as control. We have identified some interesting genes that are up- or down-regulated by BCR-ABL in these leukemia stem cells. We are currently studying the functions of these identified genes."'
GSE10912_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Bone marrow cells are isolated from the long bones of CML mice that are untreated or treated with imatinib. BCR-ABL-expressing or non-BCR-ABL-expressing (transduced with the empty GFP vector) hematopoietic stem cells (GFP+Lin-c-Kit+Sca-1+) are stored by FACS directly into RNAlater (Ambion, Austin, TX) and are homogenized in RLT Buffer (RNeasy Micro Kit (Qiagen, Valencia, CA)). Total RNA is isolated by following the protocol for the RNeasy Micro Kit, and quality is assessed using a 2100 Bioanalyzer instrument and RNA 6000 Pico LabChip assay (Agilent Technologies, Palo Alto, CA). Utilizing the GeneChip Whole Transcript Sense Target Labeling Assay kit (Affymetrix, Santa Clara, CA.) between 100-300ng of total RNA undergoes reverse transcription with random hexamers tagged with T7 sequence.  The double stranded cDNA that is generated is then amplified by T7 RNA polymerase to produce cRNA.  Second cycle first strand cDNA synthesis then takes place incorporating dUTP which is later used as sites where fragmentation occurs by utilizing an uracil DNA glycosylase and apurinic/apyrimidinic endonuclease 1 enzyme mix.  The fragmented cDNA is then labeled by terminal transferase attaching a biotin molecule using Affymetrix proprietary DNA labeling Reagent.  Approximately 2.0µg of fragmented and biotin-labeled cDNA is then hybridized onto a Mouse Gene ST 1.0 Array (Affymetrix, Santa Clara, CA.) for 16 hours at 45°C.  Post-hybridization staining and washing are performed according to manufacturer's protocols using the Fluidics Station 450 instrument (Affymetrix). Finally, the arrays are scanned with a GeneChip? Scanner 3000.  Images are acquired and cel files generated which are then used for analysis."'
GSE10912_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Bone marrow cells are isolated from the long bones of CML mice that are untreated or treated with imatinib. BCR-ABL-expressing or non-BCR-ABL-expressing (transduced with the empty GFP vector) hematopoietic stem cells (GFP+Lin-c-Kit+Sca-1+) are stored by FACS directly into RNAlater (Ambion, Austin, TX) and are homogenized in RLT Buffer (RNeasy Micro Kit (Qiagen, Valencia, CA)). Total RNA is isolated by following the protocol for the RNeasy Micro Kit, and quality is assessed using a 2100 Bioanalyzer instrument and RNA 6000 Pico LabChip assay (Agilent Technologies, Palo Alto, CA). Utilizing the GeneChip Whole Transcript Sense Target Labeling Assay kit (Affymetrix, Santa Clara, CA.) between 100-300ng of total RNA undergoes reverse transcription with random hexamers tagged with T7 sequence.  The double stranded cDNA that is generated is then amplified by T7 RNA polymerase to produce cRNA.  Second cycle first strand cDNA synthesis then takes place incorporating dUTP which is later used as sites where fragmentation occurs by utilizing an uracil DNA glycosylase and apurinic/apyrimidinic endonuclease 1 enzyme mix.  The fragmented cDNA is then labeled by terminal transferase attaching a biotin molecule using Affymetrix proprietary DNA labeling Reagent.  Approximately 2.0µg of fragmented and biotin-labeled cDNA is then hybridized onto a Mouse Gene ST 1.0 Array (Affymetrix, Santa Clara, CA.) for 16 hours at 45°C.  Post-hybridization staining and washing are performed according to manufacturer's protocols using the Fluidics Station 450 instrument (Affymetrix). Finally, the arrays are scanned with a GeneChip? Scanner 3000.  Images are acquired and cel files generated which are then used for analysis."'
GSE10915_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Comparative analysis of gene expression in ob/ob leptin-treated and ob/ob saline-treated lungs."'
GSE10915_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We hypothesize that gene expression in the lungs of these differentially-treated mice are divergent thus contributing to the disparity in their phenotypes. More specifically, (1) Effects of Leptin-treatment of ob/ob postnatal mice lungs are known to be volume-dependent from 2 to 10 wks of age, and are independent of the hypometabolism associated with leptin deficiency. ; (2) Leptin is critical to postnatal lung remodeling, particularly related to enlarged alveolar surface area. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between lungs of leptin or saline-treated ob/ob postnatal mice."'
GSE10954_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"The transcriptional regulator c-Myc is the most frequently deregulated oncogene in human tumors. Targeted overexpression of this gene in mice results in distinct types of lung adenocarcinomas. By using microarray technology, alterations in the expression of genes were captured based on a female transgenic mouse model in which, indeed, c-Myc overexpression in alveolar epithelium results in the development of bronchiolo-alveolar carcinoma (BAC) and papillary adenocarcinoma (PLAC)."'
GSE10954_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In this study, we analyzed exclusively the promoters of induced genes by different in silico methods in order to elucidate the c-Myc transcriptional regulatory network."'
GSE10962_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Herpes simplex virus mutants lacking the vhs gene are severely attenuated in animal models of pathogenesis and exhibit reduced growth in primary cell culture. As a result of these properties vhs-deleted virus have been proposed as live-attenuated viruses. Despite these findings and their implications for vacccines, the mechanisms by which vhs promotes infection in cell culture and in vivo are not understood. In this study we demonstrate that vhs-deficent viruses replicate to reduced levels in interferon(IFN)- primed cells. Furthermore, vhs-defective viruses induce increased levels of IFNβ and IFNβ-stimulated genes, and increased levels of eIF2α phosphorylation in infected cells. In addition, we demonstrate a generalized over-expression of viral RNAs following infection with a vhs-deficient virus. This suggests increased expression of IFN pathway inducing double stranded RNA, a potent pathogen-associated molecular pattern (PAMP). Together these data show that vhs likely functions to reduce innate immune responses and thereby acts as critical determinant of viral pathogenesis."'
GSE10964-GPL1261_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus."'
GSE10964-GPL339_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus."'
GSE10964-GPL340_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus."'
GSE11005_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Pneumocystis is a pathogen of immunocompromised hosts but can also infect healthy hosts, in whom infection is rapidly controlled and cleared. To better understand the immune mechanisms contributing to clearance of infection, microarray methods were used to examine differential gene expression in the lungs of  C57BL/6 and CD40 ligand knock-out (CD40L-KO) mice over time following exposure to Pneumocystis. Immuncompetent C57BL/6 mice, which control and clear infection efficiently, showed a robust response to infection characterized by the upregulation of 349 primarily immune-response associated genes.  Temporal changes in the expression of these genes suggested that there was an early (week 2) primarily innate response, that waned without controlling infection; this were followed by primarily adaptive immune responses that peaked at week 5 and successfully cleared the infection. In conjunction with the latter, there was an increased expression of B cell associated (immunoglobulin) genes at week 6 that persisted through 11 weeks.   In contrast, CD40L-KO mice, which are highly susceptible to developing severe Pneumocystis pneumonia, showed essentially no upregulation of immune-response associated genes at days 35 to 75. Immunohistochemical staining supported these observations by demonstrating an increase in CD4+, CD68+, and CD19+ cells in C57BL/6 but not CD40L-KO mice. Thus, the healthy host demonstrates a robust biphasic response to infection by Pneumocystis; CD40 ligand is an essential upstream regulator of the adaptive immune responses that efficiently control infection and prevent development of progressive pneumonia."'
GSE11005_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"In experiment 1, C57BL/6 and CD40L-KO mice were co-housed in 2 cages; one cage was exposed to a P. murina-infected seeder, while the second was unexposed. Mice (3 per group) were sacrificed at day 32. Because the initial study demonstrated very little change in gene expression in CD40L-KO mice, only C57BL/6 mice were used for experiments 2 and 3. In Experiment 2,  three cages (10 animals/cage) were set up: 2 cages were exposed to P. murina, and one was unexposed. Animals (5 per cage) were sacrificed at days 34 and 41. In Experiment 3, which focused on gene expression early after exposure to P. murina, five cages (9-10 animals/cage) were set up, of which 3 were exposed and 2 were unexposed. Animals (1-3 per cage) were sacrificed at days 7, 14 and 21 of exposure. Experiment 4 was designed to verify the initial results in CD40L-KO mice, and included 5 unexposed controls and 4 mice exposed for  35 days."'
GSE11018_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Familial pulmonary arterial hypertension (fPAH) is associated with mutations in BMPR2. Many of these mutations occur in the BMPR2 tail domain, leaving the SMAD functions intact. In order to determine the in vivo consequences of BMPR2 tail domain mutation, we created a smooth-muscle specific doxycycline inducible BMPR2 mutation with an arginine to termination mutation at amino acid 899. When these SM22-rtTA x TetO7-BMPR2R899X mice had transgene induced for 9 weeks, starting at 4 weeks of age, they universally developed pulmonary vascular pruning as assessed by fluorescent microangiography. Approximately half the time the induced animals developed elevated right ventricular systolic pressures (RVSP), associated with extensive pruning, muscularization of small pulmonary vessels, and development of large structural pulmonary vascular changes. These lesions included large numbers of macrophages and T-cells in their adventitial compartment, as well as CD133 positive cells in the lumen. Small vessels filled with CD45 positive and sometimes CD3 positive cells were a common feature in all SM22-rtTA x TetO7-BMPR2R899X mice. Gene array experiments show changes in stress response, muscle organization and function, proliferation and apoptosis, and developmental pathways before RVSP increases. Our results show that the primary phenotypic result of BMPR2 tail domain mutation in smooth muscle is pulmonary vascular pruning leading to elevated RVSP, associated with early dysregulation in multiple pathways with clear relevance to PAH. This model should be useful to the research community in examining early molecular and physical events in the development of PAH, and as a platform to validate potential treatments."'
GSE11037_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"We examined the impact of chronic lung inflammation on the pulmonary transcriptional response to inhaled urban particles.  Transcript levels were measured using high density microarrays in total RNA isolated from whole lungs of wildtype and TNF-α overexpressing mice exposed by inhalation to particulate matter and euthanized immediately or 24 h post-exposure."'
GSE11037_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"We examined the impact of chronic lung inflammation on the pulmonary transcriptional response to inhaled urban particles.  Transcript levels were measured using high density microarrays in total RNA isolated from whole lungs of wildtype and TNF-α overexpressing mice exposed by inhalation to particulate matter and euthanized immediately or 24 h post-exposure."'
GSE11037_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"Transgenic SP-C/TNF-α mice and their wildtype littermates were exposed by inhalation to particulate matter (0, 42 mg/m3 EHC-93) for 4 h and euthanized immediately or 24 h post-exposure (n=5 per treatment per time point, 40 animals total).  Agilent 22K oligonucleotide microarrays were used to examine transcript levels in whole lung RNA.  Stratagene Universal Mouse RNA was used as a reference."'
GSE11039_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We have used primary MEFs derived from wild type and E2F4 null mice growing asynchrounously in serum to generate a signature for E2F4 pathway activation.  10 wild type and 10 E2F4 null samples were each assayed using the Affymetrics Mouse Genome 430A 2.0 array."'
GSE11044-GPL1261_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We assess the concordance of histone H3 lysine 4 dimethylation (H3K4me2) and trimethylation (H3K4me3) on a genome-wide scale in erythroid development by analyzing pluripotent,  multipotential and unipotent cell types. Although H3K4me2 and H3K4me3 are concordant at most genes, multipotential hematopoietic cells have a subset of genes that are differentially methylated (H3K4me2+/me3-). These genes are transcriptionally silent, highly enriched in lineage-specific hematopoietic genes, and uniquely susceptible to differentiation-induced H3K4 demethylation.  Self-renewing embryonic stem cells, which restrict H3K4 methylation to genes that contain CpG islands (CGIs), lack H3K4me2+/me3- genes. These data reveal distinct epigenetic regulation of CGI and non-CGI genes during development and indicate an interactive relationship between DNA sequence and differential H3K4 methylation in lineage-specific differentiation."'
GSE11044-GPL6691_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We assess the concordance of histone H3 lysine 4 dimethylation (H3K4me2) and trimethylation (H3K4me3) on a genome-wide scale in erythroid development by analyzing pluripotent,  multipotential and unipotent cell types. Although H3K4me2 and H3K4me3 are concordant at most genes, multipotential hematopoietic cells have a subset of genes that are differentially methylated (H3K4me2+/me3-). These genes are transcriptionally silent, highly enriched in lineage-specific hematopoietic genes, and uniquely susceptible to differentiation-induced H3K4 demethylation.  Self-renewing embryonic stem cells, which restrict H3K4 methylation to genes that contain CpG islands (CGIs), lack H3K4me2+/me3- genes. These data reveal distinct epigenetic regulation of CGI and non-CGI genes during development and indicate an interactive relationship between DNA sequence and differential H3K4 methylation in lineage-specific differentiation."'
GSE11044-GPL6692_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We assess the concordance of histone H3 lysine 4 dimethylation (H3K4me2) and trimethylation (H3K4me3) on a genome-wide scale in erythroid development by analyzing pluripotent,  multipotential and unipotent cell types. Although H3K4me2 and H3K4me3 are concordant at most genes, multipotential hematopoietic cells have a subset of genes that are differentially methylated (H3K4me2+/me3-). These genes are transcriptionally silent, highly enriched in lineage-specific hematopoietic genes, and uniquely susceptible to differentiation-induced H3K4 demethylation.  Self-renewing embryonic stem cells, which restrict H3K4 methylation to genes that contain CpG islands (CGIs), lack H3K4me2+/me3- genes. These data reveal distinct epigenetic regulation of CGI and non-CGI genes during development and indicate an interactive relationship between DNA sequence and differential H3K4 methylation in lineage-specific differentiation."'
GSE11056_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone."'
GSE11105_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"We generated transgenic mice expressing constitutively SOCS-3 specifically in skeletal muscle. SOCS proteins are implicated in the negative regulation of various pathways including insulin signaling pathway. Our transgenic mice are predisposed to obesity and systemic insulin resistance compared to control mice."'
GSE11112_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The Forkhead Box f1 (Foxf1) transcriptional factor (previously known as HFH-8 or Freac-1) is expressed in endothelial and smooth muscle cells in the embryonic and adult lung. To assess effects of Foxf1 during lung injury, we used CCl4 injury model.  Foxf1+/- mice developed severe airway obstruction and bronchial edema, associated with increased numbers of pulmonary mast cells and increased mast cell degranulation following injury.  Pulmonary inflammation in Foxf1+/- mice was associated with diminished expression of Foxf1, increased mast cell tryptase and increased expression of CXCL12, the latter being essential for mast cell migration and chemotaxis.  Foxf1 haploinsufficiency caused pulmonary mastocytosis and enhanced pulmonary inflammation following chemically-induced lung injury, indicating an important role for Foxf1 in the pathogenesis of pulmonary inflammatory responses."'
GSE11116_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"ISR target genes in the liver of mock-injected and AP20187-treated mice of wildtype and Atf4-/- genotype"'
GSE11116_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"The low expressing Ttr::Fv2E-Perk transgene (#58) was bred into the Atf4 knockout strain and the derivative compound heterozygous mice (in the mixed FvB/n; Swiss Webster background) were backcrossed to the Atf4+/- parental stock and Ttr::Fv2E-PERK positive siblings with Atf4+/+ and  Atf4-/- genetypes were analyzed."'
GSE11123_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_title	"Mouse liver gene expression after a single acute 2h exposure to combined acoustic and restraint stress vs. control"'
GSE11123_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer."'
GSE11123_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer."'
GSE11123_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"Two biological experiments of a single acute exposure to combined acoustic and restraint stress were performed, which consist each of an acutely stressed group and an untreated control group. Liver RNA expression profiles were analyzed using pools of 8 or 9 individual RNAs of each group."'
GSE11125_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer."'
GSE11125_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer."'
GSE11126-GPL339_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer."'
GSE11126-GPL339_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer."'
GSE11126-GPL8321_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer."'
GSE11126-GPL8321_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Stress is a powerful modulator of neuroendocrine, behavioral and immunological functions. After 4.5 days of repeated combined acoustic and restraint stress as a murine model of chronic psychological stress severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turn-over, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice .Thus, in our murine model, repeated stress caused severe metabolic dysregulations leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer."'
GSE11136_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"This study analyzes gene expression associated with papilloma development in Tg.AC v-Ha-ras transgenic mice and identifies novel genes and biological processes that may be critical to skin carcinogenesis in these mice.  Epidermal abrasion was used to synchronously induce epidermal regeneration in FVB/N wild type and transgenic Tg.AC mice.  Skin papillomagenesis was uniquely induced in Tg.AC mice, and gene expression profiling was carried out using a 22,000 element mouse DNA microarray.  Histological analysis showed that papillomas developed at a high rate by day 30 after abrasion in transgenic animals, while no papilloma developed in wild type mice.  Transgene specific differentially expressed genes were identified at day 30 post-abrasion and these genes were annotated using EASE software and literature mining.  Annotated and non-annotated genes associated with papilloma development were identified and clustering analysis revealed groups of genes that are coordinately expressed.  A number of genes associated with differentiation and development were also physically clustered on mouse chromosome 16, including 16B3 that contains several Stefins and stefin-like genes, and 16A1 containing a number of keratin associated protein genes.  Additional analyses presented here yield novel insights into the genes and processes involved in papilloma development in Tg.AC mice."'
GSE11139_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The polyglutamine expansion in huntingtin (Htt) protein is a cause of Huntington’s disease (HD).  Htt is an essential gene as  deletion of the mouse Htt gene homolog (Hdh) is embryonic lethal in mice. Therefore, in addition to elucidating the mechanisms responsible for polyQ-mediated pathology, it is also important to understand the normal function of Htt protein for both basic biology and for HD. To systematically search for a mouse Htt function, we took advantage of the Hdh +/- and Hdh-floxed mice and generated four mouse embryonic fibroblast (MEF) cells lines which contain a single copy of the Hdh gene (Hdh-HET) and four MEF lines in which the Hdh gene was deleted (Hdh-KO).   The function of Htt in calcium (Ca2+) signaling was analyzed in Ca2+ imaging experiments with generated cell lines.   We found that the cytoplasmic Ca2+ spikes resulting from the activation of inositol 1,4,5-trisphosphate receptor (InsP3R) and the ensuing mitochondrial Ca2+ signals were suppressed in the Hdh-KO cells when compared to Hdh-HET cells.  Furthermore,  in experiments with permeabilized cells we found that the InsP3-sensitivity of Ca2+ mobilization from endoplasmic reticulum was reduced in Hdh-KO cells.  These results indicated that Htt plays an important role in modulating InsP3R-mediated Ca2+ signaling.  To further evaluate function of Htt, we performed genome-wide transcription profiling of generated  Hdh-HET and Hdh-KO cells by microarray.  Our results revealed that 106 unique transcripts were downregulated by more than two-fold with p < 0.05 and 173 unique transcripts were upregulated at least two-fold with p < 0.05 in Hdh-KO cells when compared to Hdh-HET cells.  The microarray results were confirmed by quantitative real-time PCR for a number of affected transcripts.  Several signaling pathways affected by Hdh gene deletion were identified from annotation of the microarray results.   The unbiased approach used in our study provides novel and unique information about the normal function of Htt in cells, which may contribute to our understanding and treatment of HD."'
GSE11141_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_title	"Effects of NgR overexpression on the developing and mature forebrain (backm-affy-mouse-433094)"'
GSE11141_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"The lack of axonal growth after injury in the adult central nervous system (CNS) is partly due to the presence of growth-inhibitory molecules associated with myelin and the intrinsic growth-state of the injured neurons. To date, three inhibitors have been identified in myelin: Myelin- Associated Glycoprotein (MAG), Nogo A, and Oligodendrocyte-Myelin glycoprotein (OMgp). These three proteins all appear to be located in the periaxonal surface of the myelin membrane placing them in an optimal location to mediate axon-glial interaction.  In addition, the three proteins have been shown to bind the same neuronal receptor, known as the Nogo-66 receptor (NgR).  It has been hypothesized that inhibition of NgR may be a strategy to increase regeneration, plasticity and functional recovery of the lesioned central nervous system. Strong NgR mRNA expression is observed in the hippocampal pyramidal cell layers (CA1-3) and the granular layer of the dentate gyrus.  It has been shown that animals exposed to entorhinal lesions show a biphasic regulation of NgR in the hippocampus, suggesting a tightly regulated mechanism mediated by this receptor.  We have access to a transgenic model to over-express NgR in forebrain hippocampal neurons. Preliminary results have shown a phenotypic response in behavior and some molecular markers, as result of NgR overexpression.  Knowledge of what genes are reacting in this novel transgenic model may provide insights into what pathways are affected by NgR to control synaptic plasticity in normal animals and during injury."'
GSE11141_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"- Effects of NgR overexpression in the mature forebrain -"'
GSE11141_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"- Effects of NgR overexpression in the developing forebrain  -"'
GSE11141_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We will also analyze the effects of NgR overexpression in bitransgenic animals raised on water.  In these animals, the NgR transgene is expressed in the forebrain upon activation of the CamKII promoter.  Since neuronal differentiation and neuronal pathways are being formed during development, we anticipate that NgR overexpression (de)effects in these animals will be markedly different to those observed in adult animals."'
GSE11141_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"We will also analyze the effects of NgR overexpression in bitransgenic animals raised on water.  In these animals, the NgR transgene is expressed in the forebrain upon activation of the CamKII promoter.  Since neuronal differentiation and neuronal pathways are being formed during development, we anticipate that NgR overexpression (de)effects in these animals will be markedly different to those observed in adult animals."'
GSE11141_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"1) Bitransgenic +  water (through entire lifespan): The animals in this group were never treated with doxycycline, and therefore expressed the NgR transgene upon activity of the CamKII promoter."'
GSE11147_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Post-transcriptional mechanisms play an important role in the control of gene expression. RNA-binding proteins are key players in the post-transcriptional control of many neural genes and they participate in multiple processes, from RNA splicing and mRNA transport to mRNA stability and translation. Our laboratory has developed the first mouse model overexpressing a RNA-binding protein, the ELAV-like protein HuD, in the CNS under the control of the CaMKinII alpha promoter. Initial behavioral characterization of the mice revealed that they had significant learning deficits together with abnormalities in prepulse inhibition (PPI). At the molecular level, we found that the expression of the growth-associated protein GAP-43, one of the targets of HuD, was increased in the hippocampus of HuD transgenic mice. To characterize these mice further and to evaluate the utility of these animals in understanding human diseases, we propose to use DNA microarray methods."'
GSE11161_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Bladder cells were FACS sorted from newborn double transgenic mice expressing EGFP under the control of a SMGA promoter and EYFP under the control of a SMAA promoter. Total RNA was isolated and underwent 2-round amplification (Epicentre® Biotechnologies) for gene expression analysis using the Affymetrix MOE430 microarray chip."'
GSE11165_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Epithelial organs including the lung are known to possess regenerative abilities through activation of endogenous stem cell populations but the molecular pathways regulating stem cell expansion and regeneration are not well understood.  Here we show that Gata6 regulates the temporal appearance and number of bronchioalveolar stem cells (BASCs) in the lung leading to the precocious appearance of BASCs and concurrent loss in epithelial differentiation in Gata6 null lung epithelium.  This expansion of BASCs is the result of a dramatic increase in canonical Wnt signaling in lung epithelium upon loss of Gata6. Expression of the non-canonical Wnt receptor Fzd2 is down-regulated in Gata6 mutants and increased Fzd2 or decreased β-catenin expression rescues, in part, the lung epithelial defects in Gata6 mutants.  During lung epithelial regeneration, we show that canonical Wnt signaling is activated in the niche containing BASCs and forced activation of Wnt signaling leads to a dramatic increase in BASC numbers.  Moreover, Gata6 is required for proper lung epithelial regeneration and postnatal loss of Gata6 leads to increased BASC expansion and decreased differentiation.  Together, these data demonstrate that Gata6 regulated Wnt signaling controls the balance between stem/progenitor expansion and epithelial differentiation required for both lung development and regeneration."'
GSE11184_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Gamma-secretase inhibitors (GSIs), which block the activation of NOTCH receptors, are being tested in the treatment of T-cell acute lymphoblastic leukemia (T-ALL). Thus far, limited antileukemic cytotoxicity and severe gastrointestinal toxicity have restricted the clinical application of these targeted drugs. Here we show that combination therapy with GSIs plus glucocorticoids can improve the antileukemic effects of GSIs and reduce their gut toxicity in vivo. Inhibition of NOTCH1 signaling in glucocorticoid-resistant T-ALL restored glucocorticoid receptor auto-up-regulation and induced apoptotic cell death through induction of BIM expression. Additionally, cotreatment with glucocorticoids induced Ccnd2 upregulation in the gut which protected mice from the intestinal secretory metaplasia typically induced by loss of NOTCH signaling. These results support a role for glucocorticoids plus GSIs in the treatment of glucocorticoid-resistant T-ALL."'
GSE11184_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Gamma-secretase inhibitors (GSIs), which block the activation of NOTCH receptors, are being tested in the treatment of T-cell acute lymphoblastic leukemia (T-ALL). Thus far, limited antileukemic cytotoxicity and severe gastrointestinal toxicity have restricted the clinical application of these targeted drugs. Here we show that combination therapy with GSIs plus glucocorticoids can improve the antileukemic effects of GSIs and reduce their gut toxicity in vivo. Inhibition of NOTCH1 signaling in glucocorticoid-resistant T-ALL restored glucocorticoid receptor auto-up-regulation and induced apoptotic cell death through induction of BIM expression. Additionally, cotreatment with glucocorticoids induced Ccnd2 upregulation in the gut which protected mice from the intestinal secretory metaplasia typically induced by loss of NOTCH signaling. These results support a role for glucocorticoids plus GSIs in the treatment of glucocorticoid-resistant T-ALL."'
GSE11184_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Experiments analyzing the interacition of dexamethasone and the gamma-secretase inhibitor DBZ were carried out in 6-week-old C57/Black6 female mice (Jackson Laboratory). In these studies we treated mice with vehicle (DMSO) (n=2), dexamethasone (15 mg/kg) (n=2), DBZ (10 micromol/kg) (n=2) and dexamethasone (15 mg/kg) plus DBZ (10 micromol/kg) (n=2) daily by intraperitoneal injection for 5 days. At the end of the treatment, animals were euthanized and segments of the small intestine were collected and processed for RNA extraction, histological and immunohistochemical analysis."'
GSE11186_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"To investigate the molecular control of hair follicle cycling, we profiled mRNA expression in mouse dorsal skin at multiple representative time points in the synchronized second postnatal hair growth cycle and in a depilation-induced hair growth cycle. For profiling of second synchronized and depilation-induced hair growth cycle, the same upper-mid region of dorsal skin was excised from C57BL/6 mice at representative postnatal days (P). The time points for second hair growth cycle are classified into different phases of the hair growth cycle based on established morphological guidelines as follow: early anagen (P23, P25), mid anagen (P27), late anagen (P29, P34), early catagen (P37, P39), mid catagen (P41), and telogen (P44). Depilation-induced hair growth cycle by applying wax/rosin mixture on the dorsal skin of seven-week old mice (all follicles in telogen) was performed on mice. The corresponding phases of the hair growth cycle at number of days following depilation (D) is as follow: early anagen (D3), mid anagen (D5), late anagen (D8, D12), and early catagen (D17). For each time point, multiple biological replicates were profiled, with each mouse dorsal skin separately hybridized to an Affymetrix array."'
GSE11191_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Cell-array permits the maintenance of the correct phenotype of cells cultured on 500 μm islands both in static and dynamic conditions.  Immunostaining and gene expression analysis confirmed the ability for cells to proliferate and differentiate in response to changed stimuli. Microarray gene expression analysis evidenced activation of specific skeletal muscle genes like MYL2, confirmed by qRT-PCR, and troponins and tropomyosins.  "'
GSE11197_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Suppression of LPS-induced IFNg and NO in splenocytes by select E2-regulated miRNA: A novel mechanism of immune mod."'
GSE11197_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"microRNA (miRNA), recently identified, non-coding, small RNA, are emerging as key regulators in homeostasis of the immune system.  Therefore, aberrant expression of miRNA may be linked to immune dysfunction, such as in chronic inflammation and autoimmunity.  In this study, we investigated the potential role of miRNA in estrogen-mediated regulation of innate immune responses, as indicated by upregulation of LPS-induced IFNg, inducible nitric oxide synthase (iNOS), and nitric oxide in splenic lymphocytes from estrogen-treated mice.  We found that miR-146a, a negative regulator of Toll-like receptor (TLR) signaling, was decreased in freshly-isolated splenic lymphocytes from estrogen-treated mice compared to placebo controls.  Increasing the activity of miR-146a significantly inhibited LPS-induced IFNg and iNOS expression in mouse splenic lymphocytes.  Further, miRNA microarray and Real-time RT-PCR analysis revealed that estrogen selectively upregulates/downregulates the expression of miRNA in mouse splenic lymphocytes.  miR-223, which is highly upregulated by estrogen, regulates LPS-induced IFNg, but not iNOS or nitric oxide in splenic lymphocytes. Inhibition of miR-223 activity decreased LPS-induced IFNg in splenic lymphocytes from estrogen-treated mice. Our data are the first demonstrating selective regulation of miRNA expression in immune cells by estrogen and are indicative of an important role of miRNA in estrogen-mediated immune regulation. "'
GSE11197_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"microRNA (miRNA), recently identified, non-coding, small RNA, are emerging as key regulators in homeostasis of the immune system.  Therefore, aberrant expression of miRNA may be linked to immune dysfunction, such as in chronic inflammation and autoimmunity.  In this study, we investigated the potential role of miRNA in estrogen-mediated regulation of innate immune responses, as indicated by upregulation of LPS-induced IFNg, inducible nitric oxide synthase (iNOS), and nitric oxide in splenic lymphocytes from estrogen-treated mice.  We found that miR-146a, a negative regulator of Toll-like receptor (TLR) signaling, was decreased in freshly-isolated splenic lymphocytes from estrogen-treated mice compared to placebo controls.  Increasing the activity of miR-146a significantly inhibited LPS-induced IFNg and iNOS expression in mouse splenic lymphocytes.  Further, miRNA microarray and Real-time RT-PCR analysis revealed that estrogen selectively upregulates/downregulates the expression of miRNA in mouse splenic lymphocytes.  miR-223, which is highly upregulated by estrogen, regulates LPS-induced IFNg, but not iNOS or nitric oxide in splenic lymphocytes. Inhibition of miR-223 activity decreased LPS-induced IFNg in splenic lymphocytes from estrogen-treated mice. Our data are the first demonstrating selective regulation of miRNA expression in immune cells by estrogen and are indicative of an important role of miRNA in estrogen-mediated immune regulation. "'
GSE11197_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Total RNAs were isolated from freshly-isolated splenic lymphocytes from 2 pairs of placebo-and estrogen-treated mice"'
GSE11202_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"Characterization of the regulatory networks mediating TLR9 dependent gene activation in vivo"'
GSE11202_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"CpG DNA interacts with TLR9 to stimulate a broadly protective innate immune response. This study uses bioinformatic network analysis of microarray data to identify the genes and regulatory networks triggered by CpG ODN. CpG treatment induced significant gene up-regulation (p < 0.00001) in the spleen within 30 min, peaking with the activation of >500 genes at 3 hr, and declining progressively thereafter. There were reproducible changes in the pattern of gene expression over time. This was mediated by a small group of “major inducers” (IL1A, IL1B, TNF, IFNG) whose activity was modulated by several “minor inducers” (NFKB1, IL6, IL15, IL18, STAT1, STAT2). The subsequent decline in gene activation was mediated by “suppressors” (MYC, IL1RN, SOCS1, SOCS3, NFKBIA, IL10, FOS) that actively down-regulated gene expression and targeted both major and minor inducers. Thus, the regulation of TLR9 dependent gene activation involves multiple waves of stimulation mediated by a small number of “major” and “minor” inducers followed by the active inhibition of gene expression by “suppressors”."'
GSE11202_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"CpG DNA interacts with TLR9 to stimulate a broadly protective innate immune response. This study uses bioinformatic network analysis of microarray data to identify the genes and regulatory networks triggered by CpG ODN. CpG treatment induced significant gene up-regulation (p < 0.00001) in the spleen within 30 min, peaking with the activation of >500 genes at 3 hr, and declining progressively thereafter. There were reproducible changes in the pattern of gene expression over time. This was mediated by a small group of “major inducers” (IL1A, IL1B, TNF, IFNG) whose activity was modulated by several “minor inducers” (NFKB1, IL6, IL15, IL18, STAT1, STAT2). The subsequent decline in gene activation was mediated by “suppressors” (MYC, IL1RN, SOCS1, SOCS3, NFKBIA, IL10, FOS) that actively down-regulated gene expression and targeted both major and minor inducers. Thus, the regulation of TLR9 dependent gene activation involves multiple waves of stimulation mediated by a small number of “major” and “minor” inducers followed by the active inhibition of gene expression by “suppressors”."'
GSE11202_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Endotoxin-free phosphorothioate ODN were synthesized at the CBER core facility (FDA, Bethesda, MD) as previously described. Mice were injected intraperitoneal (i.p.) with 400 ìg of an equimolar mixture of CpG ODNs 1555 (GCTAGACGTTAGCGT) and 1466 (TCAACGTTGA) or control ODNs 1612 (GCTAGATGTTAGCGT) and 1471 (TCAAGCTTGA). Spleens were surgically removed from mice under sterile conditions after 0.5, 1, 3, 9, 24 hr, and/or 72 hr, diced, and stored at -800 C in RNAlater (Qiagen, Valencia, CA). Data from 4 independent experiments/time point and 4-6 untreated controls were used for all statistical analyses. Reproducibility was established by comparing gene expression profiles among similarly treated mice from independent experiments in mAdb (referenced above). Expression analyses were performed using BRB ArrayTools (Biometric Research Branch, NCI). Data were background corrected, flagged values were removed, spots in which both signals were <100 were filtered out, ratios were log base 2 transformed and lowess intensity dependent normalization was used to adjust for differences in labeling intensities of the Cy3 and Cy5 dyes (Yang et al., 2002). Analysis was restricted to genes present on >70% of the arrays after filtering. The gene expression profile of all treatment groups was compared to that of the control groups."'
GSE11210_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"ISR target genes in the liver of either LFD and HFD-treated Alb::GC mice and AP20187-treated TTR::Fv2E-PERK mice"'
GSE11210_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"The high expressing Ttr::Fv2E-Perk transgenic mice was injected by either mock or AP20187. Wildtype and Alb::GC transgenic mice were fed by either Low Fat Diet (LFD) or High Fat Diet (HFD) ."'
GSE11211_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Chronic stress is a key risk factor for a variety of diseases, but the determinants of individual stress susceptibility are still unclear. Using a recently developed paradigm for chronic social stress in mice we identified animals that were resistant or susceptible to the persistent effects of chronic stress exposure. Gene expression analysis in laser-microdissected hippocampal subfields of both groups revealed differentially regulated AMPA receptor subunits, which might affect the susceptibility of an individual to chronic social stress. To test this hypothesis, animals were treated with the AMPA receptor potentiator LY451646 or vehicle during the last 4 weeks of chronic stress exposure. Enhanced AMPA receptor function in chronically stressed animals ameliorated the lasting effects of the chronic stress exposure on physiological, neuroendocrine and behavioural parameters. Our data suggest that differences in AMPA receptor function may underlie individual stress susceptibility and support AMPA receptor potentiators as potential medication in stress-related diseases."'
GSE11211_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Chronic stress is a key risk factor for a variety of diseases, but the determinants of individual stress susceptibility are still unclear. Using a recently developed paradigm for chronic social stress in mice we identified animals that were resistant or susceptible to the persistent effects of chronic stress exposure. Gene expression analysis in laser-microdissected hippocampal subfields of both groups revealed differentially regulated AMPA receptor subunits, which might affect the susceptibility of an individual to chronic social stress. To test this hypothesis, animals were treated with the AMPA receptor potentiator LY451646 or vehicle during the last 4 weeks of chronic stress exposure. Enhanced AMPA receptor function in chronically stressed animals ameliorated the lasting effects of the chronic stress exposure on physiological, neuroendocrine and behavioural parameters. Our data suggest that differences in AMPA receptor function may underlie individual stress susceptibility and support AMPA receptor potentiators as potential medication in stress-related diseases."'
GSE11229_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Dicer-null cell lines vs. wt ES cells and Dicer-null cell lines vs. Dicer-null cells overexpressing Dnmt1 or Dnmt3a/3b"'
GSE11229_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"Dicer initiates RNA interference by generating small RNAs involved in various silencing pathways. Dicer participates in centromeric silencing, but its role in the epigenetic regulation of other chromatin domains has not been explored. Here we show that Dicer1 deficiency in Mus musculus leads to decreased DNA methylation, concomitant with increased telomere recombination and telomere elongation. These DNA-methylation defects correlate with decreased expression of Dnmt1, Dnmt3a and Dnmt3b DNA methyltransferases (Dnmts), and methylation levels can be recovered by their overexpression. We identify the retinoblastoma-like 2 protein (Rbl2) as responsible for decreased Dnmt expression in Dicer1-null cells, suggesting the existence of Dicer-dependent small RNAs that target Rbl2."'
GSE11244_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Background: Calorie restriction (CR) is the only intervention known to extend lifespan in a wide range of organisms, including mammals. However, the mechanisms by which it regulates mammalian aging remain largely unknown and the involvement of the TOR and Sirtuin pathways (which regulate aging in lower organisms) remain controversial. Femaleness is a second phenotype generally associated with longevity but the relationship between sex-biased and CR-induced gene expression remains undetermined.    Methodology/Principal Findings: We generated microarray gene expression data from livers of male mice fed high calorie or CR diets, and we find that CR significantly changes the expression of over 3,000 genes, many between 10- and 50-fold. We compare our data to the GenAge database of known aging-related genes and to prior microarray expression data of genes expressed differently between male and female mice. CR generally feminizes gene expression and many of the most significantly changed individual genes are involved in aging, hormone signaling, and p53-associated regulation of the cell cycle and apoptosis. Among the genes showing the largest and most statistically significant CR-induced expression differences are Ddit4, a key regulator of the TOR pathway, and Nnmt, a regulator of lifespan linked to the Sirtuin pathway. Using Western analyses, we confirmed post-translational inhibition of the TOR pathway.    Conclusions: Our data show that CR induces widespread gene expression changes and acts through highly evolutionarily conserved pathways, from microorganisms to mammals, and that its life-extension effects might arise partly from a shift toward a gene expression profile more typical of the longer-lived female sex."'
GSE11249_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Differentiation of 3T3-L1 preadipocytes can be induced by a 2-d treatment with a factor ""cocktail"" (DIM) containing the synthetic glucocorticoid dexamethasone (dex), insulin, the phosphodiesterase inhibitor methylisobutylxanthine (IBMX) and fetal bovine serum (FBS). We temporally uncoupled the activities of the four DIM components and found that treatment with dex for 48 h followed by IBMX treatment for 48 h was sufficient for adipogenesis, whereas treatment with IBMX followed by dex failed to induce significant differentiation. Similar results were obtained with C3H10T1/2 and primary mesenchymal stem cells. The 3T3-L1 adipocytes differentiated by sequential treatment with dex and IBMX displayed insulin sensitivity equivalent to DIM adipocytes, but had lower sensitivity to isoproterenol-stimulated lipolysis and reduced triglyceride content. The nondifferentiating IBMX–then-dex treatment produced transient expression of adipogenic transcriptional regulatory factors C/EBP{beta} and C/EBP{delta}, and little induction of terminal differentiation factors C/EBP{alpha} and PPAR{gamma}. Moreover, the adipogenesis inhibitor preadipocyte factor-1 (Pref-1) was repressed by DIM or by dex-then-IBMX, but not by IBMX-then-dex treatment. We conclude that glucocorticoids drive preadipocytes to a novel intermediate cellular state, the dex-primed preadipocyte, during adipogenesis in cell culture, and that Pref-1 repression may be a cell fate determinant in preadipocytes."'
GSE11249_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Differentiation of 3T3-L1 preadipocytes can be induced by a 2-d treatment with a factor ""cocktail"" (DIM) containing the synthetic glucocorticoid dexamethasone (dex), insulin, the phosphodiesterase inhibitor methylisobutylxanthine (IBMX) and fetal bovine serum (FBS). We temporally uncoupled the activities of the four DIM components and found that treatment with dex for 48 h followed by IBMX treatment for 48 h was sufficient for adipogenesis, whereas treatment with IBMX followed by dex failed to induce significant differentiation. Similar results were obtained with C3H10T1/2 and primary mesenchymal stem cells. The 3T3-L1 adipocytes differentiated by sequential treatment with dex and IBMX displayed insulin sensitivity equivalent to DIM adipocytes, but had lower sensitivity to isoproterenol-stimulated lipolysis and reduced triglyceride content. The nondifferentiating IBMX–then-dex treatment produced transient expression of adipogenic transcriptional regulatory factors C/EBP{beta} and C/EBP{delta}, and little induction of terminal differentiation factors C/EBP{alpha} and PPAR{gamma}. Moreover, the adipogenesis inhibitor preadipocyte factor-1 (Pref-1) was repressed by DIM or by dex-then-IBMX, but not by IBMX-then-dex treatment. We conclude that glucocorticoids drive preadipocytes to a novel intermediate cellular state, the dex-primed preadipocyte, during adipogenesis in cell culture, and that Pref-1 repression may be a cell fate determinant in preadipocytes."'
GSE11249_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"We sought to define the genes differentially expressed in response to dexamethasone (dex) in 3T3L1 mouse preadipocytes.  We treated 3T3L1 cells with dex or DMSO vehicle for 2 or 36 hrs and then prepared total RNA.  We hybridized each sample (Cy5) to a pool of the samples, which served as the reference (Cy3) channel. All linear models for differential gene expression were constructed with the ""limma"" package (Smyth, 2004) in BioConductor (Gentleman et al., 2004). A linear model for dex was constructed to compare the 4 biological replicates of DMSO vehicle treatment with dex treatment at either 2 or 36hr. Genes were considered differentially expressed if at least one probe had log-odds greater than 50:50 in the linear model."'
GSE11252_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"We used microarrays to detail the global programme of gene expression response due to MMS exposure in a DNA repair proficient or deficient mouse"'
GSE11252_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mice (WT and Aag null) were treated with MMS and livers extracted at 6, 12, 24, and 48 hours"'
GSE11253_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"We used mice that harbor floxed alleles for the Rb family and we induced the recombination by 6 weeks of age. KLS (c-Kit+ Lin - Sca-1+) cells were sorted 2 months after the recombination."'
GSE11256-GPL339_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"we used DNA microarray analysis to identify genes that are induced by neuronal activity in excitatory neurons at the time when inhibitory synapses are forming and maturing on them."'
GSE11256-GPL340_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"we used DNA microarray analysis to identify genes that are induced by neuronal activity in excitatory neurons at the time when inhibitory synapses are forming and maturing on them."'
GSE11258_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"We infected mouse hippocampal neurons with lentivirus expressing Npas4-RNAi or control-RNAi @ 3 DIV and depolarized the neurons @ 8 DIV with 50 mM of KCl for 0, 1, 3 or 6 hours. Neurons were lysed, mRNA isolated and hybridized to Affymetrix arrays. Data were collected from 3 independent experiments."'
GSE11286_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"Four mice of the Apo E (-/-) strain were exposed to diesel engine particulate from the National Institute of Standards and Technology via intratracheal instillation.  Controls consisted of 4 littermates exposed to saline vehicle.  Four wild type mice were similarly exposed to diesel particulate and four to vehicle control.  24 hours after exposure, mice were humanely sacrificed by carbon dioxide asphyxiation and the hearts and lungs were collected and frozen for analysis of total RNA.  2 color microarrays were utilized to compare pooled RNA representing all four animals of each strain, and  in each condition and in each tissue."'
GSE11288_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_title	"Gene microarray analysis of mouse-brain endothelial cells exposure to Pertussis Toxin and B-oligomer"'
GSE11288_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"MBEC(passage1) cultured on collagen-coated glass chamber slides were treated with PTX and B-oligomer at 3ng/ml, or PBS as control. Six hours later, total RNA were isolated from the cells. Gene microarray were performed to identify early candidate genes that are affected by PTX. The experiment was repeated twice independently."'
GSE11295_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"PPARγ activation promotes infiltration of alternatively activated macrophages into adipose tissue."'
GSE11295_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Background: Obesity is associated with infiltration of macrophages into adipose tissue. Adipose macrophages may contribute to an elevated inflammatory status by secreting a variety of pro-inflammatory mediators, including TNFalpha and IL-6. Recent data suggest that during diet-induced obesity the phenotype of adipose-resident macrophages changes from alternatively activated macrophages towards a more classical and pro-inflammatory phenotype. Here, we explore the effect of PPARγ-activation on obesity-induced inflammation in 129SV mice fed a high fat diet for 20 weeks. High fat feeding increased bodyweight gain, adipose tissue mass and liver triglycerides. Rosiglitazone treatment further increased adipose mass, reduced liver triglycerides and changed adipose tissue morphology towards smaller adipocytes. Surprisingly, rosiglitazone markedly increased the number of macrophages in adipose tissue, as shown by immunohistochemical analysis and quantification of macrophage marker genes CD68 and F4/80+. In adipose tissue, markers for classically activated macrophages including IL-18 were down regulated whereas markers characteristic for alternatively activated macrophages (Arginase 1, IL-10) were up regulated by rosiglitazone. Importantly, conditioned media from rosiglitazone-treated alternatively activated macrophages neutralized the inhibitory effect of macrophages on 3T3-L1 adipocyte differentiation, suggesting that alternatively activated macrophages may be involved in mediating the effects of rosiglitazone on adipose tissue morphology and mass. Our results suggest that short term rosiglitazone treatment increases infiltration of alternatively activated macrophages in adipose tissue. The alternatively activated macrophages might play a role in PPARγ-dependent expansion and remodeling of adipose tissue."'
GSE11295_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Background: Obesity is associated with infiltration of macrophages into adipose tissue. Adipose macrophages may contribute to an elevated inflammatory status by secreting a variety of pro-inflammatory mediators, including TNFalpha and IL-6. Recent data suggest that during diet-induced obesity the phenotype of adipose-resident macrophages changes from alternatively activated macrophages towards a more classical and pro-inflammatory phenotype. Here, we explore the effect of PPARγ-activation on obesity-induced inflammation in 129SV mice fed a high fat diet for 20 weeks. High fat feeding increased bodyweight gain, adipose tissue mass and liver triglycerides. Rosiglitazone treatment further increased adipose mass, reduced liver triglycerides and changed adipose tissue morphology towards smaller adipocytes. Surprisingly, rosiglitazone markedly increased the number of macrophages in adipose tissue, as shown by immunohistochemical analysis and quantification of macrophage marker genes CD68 and F4/80+. In adipose tissue, markers for classically activated macrophages including IL-18 were down regulated whereas markers characteristic for alternatively activated macrophages (Arginase 1, IL-10) were up regulated by rosiglitazone. Importantly, conditioned media from rosiglitazone-treated alternatively activated macrophages neutralized the inhibitory effect of macrophages on 3T3-L1 adipocyte differentiation, suggesting that alternatively activated macrophages may be involved in mediating the effects of rosiglitazone on adipose tissue morphology and mass. Our results suggest that short term rosiglitazone treatment increases infiltration of alternatively activated macrophages in adipose tissue. The alternatively activated macrophages might play a role in PPARγ-dependent expansion and remodeling of adipose tissue."'
GSE11295_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Background: Obesity is associated with infiltration of macrophages into adipose tissue. Adipose macrophages may contribute to an elevated inflammatory status by secreting a variety of pro-inflammatory mediators, including TNFalpha and IL-6. Recent data suggest that during diet-induced obesity the phenotype of adipose-resident macrophages changes from alternatively activated macrophages towards a more classical and pro-inflammatory phenotype. Here, we explore the effect of PPARγ-activation on obesity-induced inflammation in 129SV mice fed a high fat diet for 20 weeks. High fat feeding increased bodyweight gain, adipose tissue mass and liver triglycerides. Rosiglitazone treatment further increased adipose mass, reduced liver triglycerides and changed adipose tissue morphology towards smaller adipocytes. Surprisingly, rosiglitazone markedly increased the number of macrophages in adipose tissue, as shown by immunohistochemical analysis and quantification of macrophage marker genes CD68 and F4/80+. In adipose tissue, markers for classically activated macrophages including IL-18 were down regulated whereas markers characteristic for alternatively activated macrophages (Arginase 1, IL-10) were up regulated by rosiglitazone. Importantly, conditioned media from rosiglitazone-treated alternatively activated macrophages neutralized the inhibitory effect of macrophages on 3T3-L1 adipocyte differentiation, suggesting that alternatively activated macrophages may be involved in mediating the effects of rosiglitazone on adipose tissue morphology and mass. Our results suggest that short term rosiglitazone treatment increases infiltration of alternatively activated macrophages in adipose tissue. The alternatively activated macrophages might play a role in PPARγ-dependent expansion and remodeling of adipose tissue."'
GSE11317_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The lymphatic system is a common avenue for the spread of breast cancer cells and dissemination through it occurs at least as frequently as hematogenous metastasis. Approximately 75% of primary breast cancers are estrogen receptor (ER) positive and the majority of these maintain receptor expression as lymph node (LN) metastases. However, it is unknown if ER function is equivalent in cancer cells growing in the breast and in the LNs. We have developed a model to assess estrogen responsiveness in ER(+) breast tumors and LN metastases. Fluorescent ER(+) MCF-7 tumors were grown in ovariectomized nude mice supplemented with estradiol. Once axillary LN metastasis arose, estradiol was withdrawn (EWD), for 1 or 4 weeks, or continued, to assess estradiol responsiveness. On EWD, proliferation rates fell similarly in tumors and LN metastases. However, estradiol-dependent ER down-regulation and progesterone receptor induction were deficient in LN metastases, indicating that ER-dependent transcriptional function was altered in the LN. Cancer cells from estradiol-treated and EWD primary tumors and matched LN metastases were isolated by laser capture microdissection. Global gene expression profiling identified transcripts that were regulated by the tissue microenvironment, by hormones, or by both. Interestingly, numerous genes that were estradiol regulated in tumors lost estradiol sensitivity or were regulated in the opposite direction by estradiol in LN metastases. We propose that the LN microenvironment alters estradiol signaling and may contribute to local antiestrogen resistance."'
GSE11319_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Tyrosine kinase-activating mutations in Met have been observed in hereditary papillary renal carcinomas as well as in other cancers. These mutations have been examined in several in vitro systems, where they cause constitutive Met activation, focus formation, and cell motility, and are tumorigenic in xenografts. To determine the influence of these mutations on tumorigenesis in vivo, we generated mice with targeted mutations in the murine met locus. Five mouse lines with mutant Met were created: wt, D1226N, Y1228C, M1248T, and M1248T/L1193V. These mouse lines develop a wide range of sarcomas, lymphomas, and carcinomas. To determine if mutationally activated forms of Met have altered signaling specificity we utilized gene expression analysis. Mouse embryonic fibroblasts (MEFs) were isolated from the mutant Met lines and here we present data for wild type and M1248T (M833). Our results indicate that Met activating mutations have unique gene expression signatures."'
GSE11322_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"XBP1 is a transcription factor that is induced by unconventional splicing associated with endoplasmic reticulum stress and plays a role in development of liver and plasma cells. We previously reported that brain derived neurotrophic factor (BDNF) leads to splicing of XBP1 mRNA in neurites, and that XBP1 is required for BDNF-induced neurite extension and branching. To search for the molecular mechanisms of how XBP1 plays a role in neural development, comprehensive gene expression analysis was performed in primary telencephalic neurons obtained from Xbp1 knockout mice at embryonic day 12.5. By searching for the genes induced by BDNF in wild type neurons but this induction was reduced in Xbp1 knockout mice, we found that upregulation of three GABAergic markers, somatostatin (Sst), neuropeptide Y (Npy), and calbindin (Calb1), were compromised in Xbp1 knockout neurons. Attenuated induction of Npy and Calb1 was confirmed by quantitative RT-PCR. In neurons lacking in Xbp1, upregulation of GABAergic markers was attenuated.  Impaired BDNF-induced neurite extension in Xbp1 knockout neurons might be mediated by disturbed BDNF-induced differentiation of GABAergic interneurons."'
GSE11322_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Two female Xbp1 +/- mice were mated with male Xbp1 +/- mice, and at embryonic day 12.5 (E12.5) the embryos were dissected. Among the 25 embryos obtained from the 2 pregnant female mice, 6 were genotyped as Xbp1 -/- and 4 were Xbp1 +/+ by a rapid PCR assay using Z-Taq. Telencephalon was dissected from each embryo, and treated with collagenase and trypsin. Six Xbp1 -/- telencephalon samples and 4 Xbp1 +/+ samples were collected together, respectively. Each sample was divided into 15 aliquots, and the cells were subject to low density culture on plastic culture dishes. The neurons were maintained in a serum-free medium (Neurobasal medium supplemented with 0.5 mM glutamine and B27 supplement [Invitrogen]). On the third day in vitro (3 DIV) , neurons in 10 of 15 dishes in each group were stimulated with BDNF (100 ng/ml). On 4 DIV, neurons in 5 dishes stimulated with BDNF (24 hours BDNF treatment) and 5 dishes with no stimulation (0 hour) were lysed to extract total RNA. On 5 DIV, neurons in 5 dishes stimulated with BDNF (48 hours BDNF treatment) were lysed."'
GSE11322_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Two female Xbp1 +/- mice were mated with male Xbp1 +/- mice, and at embryonic day 12.5 (E12.5) the embryos were dissected. Among the 25 embryos obtained from the 2 pregnant female mice, 6 were genotyped as Xbp1 -/- and 4 were Xbp1 +/+ by a rapid PCR assay using Z-Taq. Telencephalon was dissected from each embryo, and treated with collagenase and trypsin. Six Xbp1 -/- telencephalon samples and 4 Xbp1 +/+ samples were collected together, respectively. Each sample was divided into 15 aliquots, and the cells were subject to low density culture on plastic culture dishes. The neurons were maintained in a serum-free medium (Neurobasal medium supplemented with 0.5 mM glutamine and B27 supplement [Invitrogen]). On the third day in vitro (3 DIV) , neurons in 10 of 15 dishes in each group were stimulated with BDNF (100 ng/ml). On 4 DIV, neurons in 5 dishes stimulated with BDNF (24 hours BDNF treatment) and 5 dishes with no stimulation (0 hour) were lysed to extract total RNA. On 5 DIV, neurons in 5 dishes stimulated with BDNF (48 hours BDNF treatment) were lysed."'
GSE11333_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_title	"ELAV-like protein HuD overexpression and pulldown (perro-affy-mouse-482241)"'
GSE11333_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Post-transcriptional mechanisms play an important role in the control of gene expression. RNA-binding proteins are key players in the post-transcriptional control of many neural genes and they participate in multiple processes, from RNA splicing and mRNA transport to mRNA stability and translation. Our laboratory has developed the first mouse model overexpressing a RNA-binding protein, the ELAV-like protein HuD, in the CNS under the control of the CaMKinII alpha promoter. Initial behavioral characterization of the mice revealed that they had significant learning deficits together with abnormalities in prepulse inhibition (PPI). At the molecular level, we found that the expression of the growth-associated protein GAP-43, one of the targets of HuD, was increased in the hippocampus of HuD transgenic mice."'
GSE11343_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Rosiglitazone Treatment Reduces Diabetic Neuropathy in STZ treated DBA/2J mice"'
GSE11343_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Diabetic Neuropathy (DN) is a common complication of diabetes.  Currently, there is no drug treatment to prevent or slow the development of DN.  Rosiglitazone (Rosi) is a potent insulin sensitizer and may also slow the development of DN by a mechanism independent of its effect on hyperglycemia.  A two by two design was used to test the effect of Rosi treatment on the development of DN.  Streptozotocin-induced diabetic DBA/2J mice were treated with Rosi.  DN and oxidative stress were quantified, and gene expression was profiled using the Affymetrix Mouse Genome 430 2.0 microarray platform.  An informatics approach identified key regulatory elements activated by Rosi.  Diabetic DBA/2J mice developed severe hyperglycemia, DN and elevated oxidative stress.  Rosi treatment did not affect hyperglycemia but did reduce oxidative stress and prevented development of thermal hypoalgesia.  Two novel transcription factor binding modules were identified that may control genes correlated to changes in DN following Rosi treatment: SP1F_ZBPF and EGRF_EGRF.  Rosi treatment reduced oxidative stress and DN independent of its insulin sensitizing effects. Gene expression profiling identified two novel targets activated by Rosi treatment.  These targets may be useful in designing drugs with the same efficacy as Rosi in treating DN but with fewer undesirable effects."'
GSE11343_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Diabetic Neuropathy (DN) is a common complication of diabetes.  Currently, there is no drug treatment to prevent or slow the development of DN.  Rosiglitazone (Rosi) is a potent insulin sensitizer and may also slow the development of DN by a mechanism independent of its effect on hyperglycemia.  A two by two design was used to test the effect of Rosi treatment on the development of DN.  Streptozotocin-induced diabetic DBA/2J mice were treated with Rosi.  DN and oxidative stress were quantified, and gene expression was profiled using the Affymetrix Mouse Genome 430 2.0 microarray platform.  An informatics approach identified key regulatory elements activated by Rosi.  Diabetic DBA/2J mice developed severe hyperglycemia, DN and elevated oxidative stress.  Rosi treatment did not affect hyperglycemia but did reduce oxidative stress and prevented development of thermal hypoalgesia.  Two novel transcription factor binding modules were identified that may control genes correlated to changes in DN following Rosi treatment: SP1F_ZBPF and EGRF_EGRF.  Rosi treatment reduced oxidative stress and DN independent of its insulin sensitizing effects. Gene expression profiling identified two novel targets activated by Rosi treatment.  These targets may be useful in designing drugs with the same efficacy as Rosi in treating DN but with fewer undesirable effects."'
GSE11344_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Short hairpin knockdown of PTB in mouse N2A neuroblastoma cells was performed as described before (Boutz et al., 2007, Genes Dev 21:1636-1652). The efficiency of the PTB knockdown was monitored by western blot using PTB-NT primary antibody and Cy5 labeled secondary antibody (GE Life Sciences). The blots were imaged using Typhoon 9410 (GE Life Sciences). The band intensities were measured using ImageQuant and normalized to GAPDH. In all cases the efficiency of the knockdown was close to 80% (data not shown). We conducted Exon array profiling on RNAs from three shRNA-PTB treated samples and three mock-treated controls (using empty vectors)."'
GSE11346_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Serum amyloid and serum amyloid P are not induced in response to diesel exhaust particles or carbon black"'
GSE11346_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"W evaluated an experimental particle exposure model, including markers of the acute phase system assessed as the hepatic mRNA expression of Sap, the murine homologue of CRP, and Saa1 and Saa3."'
GSE11357_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Radiotherapy is widely used to treat human cancer. Patients locally recurring after radiotherapy, however, have increased risk of metastatic progression and poor prognosis. The clinical management of post-radiation recurrences remains an unresolved issue. Tumors growing in pre-irradiated tissues have an increased fraction of hypoxic cells and are more metastatic, a condition known as tumor bed effect. Here we demonstrate that tumor cells growing in a pre-irradiated bed, or selected in vitro though repeated cycles of severe hypoxia, retain an invasive and metastatic capacities when returned to normoxia. HIF activity, while it facilitates metastatic spreading of tumors growing in a pre-irradiated bed, is not essential. Through gene expression profiling and gain and loss of function experiments, we identified the matricellular protein CYR61 and aVb5 integrin, as proteins cooperating to mediate these effects. Inhibition of aVb5 integrin suppressed invasion and metastasis induced by CYR61 and attenuated metastasis of tumors growing within a pre-irradiated field. These results represent a conceptual advance to the understanding of the tumor bed effect and identify CYR61 and aVb5 integrin as proteins that co-operate to mediate metastasis. They also indicate aV integrin inhibition a potential therapeutic approach for preventing metastasis in patients at risk for post-radiation recurrences, which can be promptly tested in the clinic."'
GSE11371_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Current knowledge of mechanically-induced regulation of gene expression in fibroblast is mostly based on experiments using prolonged cyclical stretching of either cultured cells or load-bearing connective tissues such as tendons and ligaments.  In this study, we have examined the effect of static tissue stretch on fibroblasts within loose connective tissue using in vivo and ex vivo models.   In an in vivo trunk side bending model, one side of the trunk of the mouse was stretched while the other side was shortened under anesthesia for 90 minutes. In the ex vivo method, whole subcutaneous tissue explants (including skin, subcutaneous muscle and subcutaneous tissue) from both sides of the trunk were incubated ex vivo either stretched or not stretched (shortened) for 24 hours.  Tissue stretch or shortening was followed by immediate dissection of the loose connective tissue layer on both sides of the trunk, RNA extraction and gene expression analysis using Affymetrix mouse gene arrays.  In both in vivo and ex vivo experiments, a large cluster of genes related to skeletal muscle function and carbohydrate metabolism was up-regulated in the stretched, compared with the shortened, connective tissue samples.  However, there were few differentially expressed matrix-related genes, and in particular no change in collagen genes.  Immunohistochemical staining for myosin after tissue stretch for 24 hours ex vivo showed increased myosin immunoreactivity in fibroblasts within the stretched compared with the shortened tissue samples. These results suggest that dynamic modulation of muscle-related gene expression is a normal physiological response of loose connective tissue fibroblasts to changes in tissue length.."'
GSE11382_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We evaluated aflatoxin B1-induced liver tumor promotion by H. hepaticus. Microarrays of liver and cecum from female mice were used to evaluate the individual and combined transcriptional effects of AFB1 and H. hepaticus"'
GSE11398-GPL81_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Expression profiling in transgenic FVB/N embryonic stem cells overexpressing STAT3. "'
GSE11398-GPL81_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"To investigate the importance of STAT3 in the establishment of ES cells we have in a first step derived stable pluripotent embryonic stem cells from transgenic FVB mice expressing a conditional tamoxifen dependent STAT3-MER fusion protein. In a second step, STAT3-MER overexpressing cells were used to identify STAT3 pathway-related genes by expression profiling in order to identify new key-players involved in maintenance of pluripotency in ES cells."'
GSE11398-GPL81_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"To investigate the importance of STAT3 in the establishment of ES cells we have in a first step derived stable pluripotent embryonic stem cells from transgenic FVB mice expressing a conditional tamoxifen dependent STAT3-MER fusion protein. In a second step, STAT3-MER overexpressing cells were used to identify STAT3 pathway-related genes by expression profiling in order to identify new key-players involved in maintenance of pluripotency in ES cells."'
GSE11398-GPL81_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_overall_design	"FVB/N derived embryonic stem cells cultivated in the presence of LIF were compared with FVB/N ES cells overexpressing STAT3-MER and cultivated in the presence of 4-hydroxytamoxifen and absence of LIF"'
GSE11398-GPL82_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Expression profiling in transgenic FVB/N embryonic stem cells overexpressing STAT3. "'
GSE11398-GPL82_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"To investigate the importance of STAT3 in the establishment of ES cells we have in a first step derived stable pluripotent embryonic stem cells from transgenic FVB mice expressing a conditional tamoxifen dependent STAT3-MER fusion protein. In a second step, STAT3-MER overexpressing cells were used to identify STAT3 pathway-related genes by expression profiling in order to identify new key-players involved in maintenance of pluripotency in ES cells."'
GSE11398-GPL82_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"To investigate the importance of STAT3 in the establishment of ES cells we have in a first step derived stable pluripotent embryonic stem cells from transgenic FVB mice expressing a conditional tamoxifen dependent STAT3-MER fusion protein. In a second step, STAT3-MER overexpressing cells were used to identify STAT3 pathway-related genes by expression profiling in order to identify new key-players involved in maintenance of pluripotency in ES cells."'
GSE11398-GPL82_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_overall_design	"FVB/N derived embryonic stem cells cultivated in the presence of LIF were compared with FVB/N ES cells overexpressing STAT3-MER and cultivated in the presence of 4-hydroxytamoxifen and absence of LIF"'
GSE11398-GPL83_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Expression profiling in transgenic FVB/N embryonic stem cells overexpressing STAT3. "'
GSE11398-GPL83_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"To investigate the importance of STAT3 in the establishment of ES cells we have in a first step derived stable pluripotent embryonic stem cells from transgenic FVB mice expressing a conditional tamoxifen dependent STAT3-MER fusion protein. In a second step, STAT3-MER overexpressing cells were used to identify STAT3 pathway-related genes by expression profiling in order to identify new key-players involved in maintenance of pluripotency in ES cells."'
GSE11398-GPL83_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"To investigate the importance of STAT3 in the establishment of ES cells we have in a first step derived stable pluripotent embryonic stem cells from transgenic FVB mice expressing a conditional tamoxifen dependent STAT3-MER fusion protein. In a second step, STAT3-MER overexpressing cells were used to identify STAT3 pathway-related genes by expression profiling in order to identify new key-players involved in maintenance of pluripotency in ES cells."'
GSE11398-GPL83_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_overall_design	"FVB/N derived embryonic stem cells cultivated in the presence of LIF were compared with FVB/N ES cells overexpressing STAT3-MER and cultivated in the presence of 4-hydroxytamoxifen and absence of LIF"'
GSE11434_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Ventilator-induced lung injury in C57BL\6 mice"'
GSE11434_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"This study was undertaken to examine differential gene expression across the whole genome during short-term ventilator-induced lung injury in mice, a commonly used model of acute lung injury, as compared with spontaneous ventilation. "'
GSE11434_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mice were anesthetized with isoflurane followed by ketamine/xylaxine. Saline (0.25 ml) was given every hour ip. A tracheotomy tube was placed and the mice were ventilated with an initial peak airway pressure of 20 cmH2O approximating a tidal volume of 20 ml/kg and without end-expiratory pressure. Ventilation was continued for 3h. Tidal volume was not adjusted. Body temperature was monitored with a digital rectal thermometer and maintained at 37C with a heating table and external heating lamp. Control mice were treated identically, but were not mechanically ventilated (i.e. breathed spontaneously). There were 5 biological relicates in each group."'
GSE11446_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"CD8 T cells stimulated with IL-2 complex in vivo"'
GSE11449_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"RAW264.7 cells were treated with KDO, IFN beta and 8Br"'
GSE11449_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"RAW 264.7 cells were stimulated with KDO (100 ng/ml), IFN-β (300 pM) and/or 8-Br 100 μM. These ligands were applied individually or in combination with KDO for 60 min and 120 min. Total RNA was extracted using TriPure (Roche) following its protocol. "'
GSE11449_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"RAW 264.7 cells were stimulated with KDO (100 ng/ml), IFN-β (300 pM) and/or 8-Br 100 μM. These ligands were applied individually or in combination with KDO for 60 min and 120 min. Total RNA was extracted using TriPure (Roche) following its protocol. The detailed procedure is available at http://www.signaling-gateway.org/data/ProtocolLinks.html (AfCS Procedure Protocol PP00000009). Duplicate experiments were done for each treatment. "'
GSE11449_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	" The hybridization experiment and analysis were performed as previously described (Park et al., 2004; Zhu et al., 2006; Zhu et al., 2004). Cy5-labeled cRNA (RNA of ligand treated cells) and Cy3-labeled cRNA (RNA of time matched controls) were hybridized in the array. Dye-swap labeling was performed for each pair of samples. The arrays were scanned with Agilent Scanner G2505A (Agilent Technologies) and image files were extracted with background subtraction and dye-normalization using Agilent G2566AA Extraction Software version A.6.1.1 (Agilent Technologies)."'
GSE11484_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Understanding the nature of the various glucose-derived signals for insulin secretion (both triggering and amplifying) is essential for gaining insight into the functional failure of the beta-cells in diabetes and the development of drugs for correcting this problem. The beta-cells uniquely couple changes in cellular metabolism to electrical activity and thus insulin release. In mice, beta-cell specific deletion of the von Hippel-Lindau (VHL) tumor suppressor protein leads to the activation of a HIF transcription program that includes genes involved in glycolysis, suppression of mitochondrial activity and lactate production. This reprogramming of cellular metabolism results in abnormal insulin secretion properties."'
GSE11494_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Streptococcus pyogenes is a major causative agent of tonsillitis or pharyngitis in children, which can lead to more invasive infections and noninfectious sequellae. S. pyogenes can persist in tonsils, while one-third of children treated with antibiotics continue to shed streptococci and have recurrent infections. Mouse nasal-associated lymphoid tissue (NALT) is functionally analogous to human oropharangeal lymphoid tissues. The innate immune responses of naïve cells from a mucosal site to S. pyogenes is not well described; therefore, we infected C57BL/6 mice intranasally with 108 CFU S. pyogenes. Transcriptional responses by NALT after S. pyogenes infection were analyzed by Affymetrix microarray and quantitative RT-PCR.  Wild-type S. pyogenes induces transcription of both type I and IFN-gamma-responsive genes, pro-inflammatory genes, and acute phase response plasma proteins within 24h after infection.   Invasion of NALT and the induction of the interferon response were not dependent on expression of anti-phagocytic M1 protein.  However, infection with an attenuated, less invasive mutant indicated that a robust innate response by NALT is significantly influenced by intra-NALT bacterial load.  Granulocytic populations of NALT, cervical lymph nodes and spleen were discriminated by characteristic surface and intracellular markers.  Intranasal infection induces systemic release of neutrophils and a substantial influx of neutrophils into NALT at 24h, which decline by 48h after infection.  Macrophages do not significantly increase in S. pyogenes-infected NALT.  Intranasal infection of IFN-gamma -/- (GKO) C57BL/6 mice did not lead to systemic dissemination of wild type S. pyogenes, despite reduced expression of IFN-gamma-responsive mRNAs in NALT.   Infected GKO mice had an unregulated influx of neutrophils into NALT compared to immunocompetant mice and mice treated with an anti-IFN-gamma antibody more rapidly cleared S. pyogenes from NALT.  Thus, IFN-gamma-induced responses have a suppressive influence on early clearance of this pathogen from NALT."'
GSE11494_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Streptococcus pyogenes is a major causative agent of tonsillitis or pharyngitis in children, which can lead to more invasive infections and noninfectious sequellae. S. pyogenes can persist in tonsils, while one-third of children treated with antibiotics continue to shed streptococci and have recurrent infections. Mouse nasal-associated lymphoid tissue (NALT) is functionally analogous to human oropharangeal lymphoid tissues. The innate immune responses of naïve cells from a mucosal site to S. pyogenes is not well described; therefore, we infected C57BL/6 mice intranasally with 108 CFU S. pyogenes. Transcriptional responses by NALT after S. pyogenes infection were analyzed by Affymetrix microarray and quantitative RT-PCR.  Wild-type S. pyogenes induces transcription of both type I and IFN-gamma-responsive genes, pro-inflammatory genes, and acute phase response plasma proteins within 24h after infection.   Invasion of NALT and the induction of the interferon response were not dependent on expression of anti-phagocytic M1 protein.  However, infection with an attenuated, less invasive mutant indicated that a robust innate response by NALT is significantly influenced by intra-NALT bacterial load.  Granulocytic populations of NALT, cervical lymph nodes and spleen were discriminated by characteristic surface and intracellular markers.  Intranasal infection induces systemic release of neutrophils and a substantial influx of neutrophils into NALT at 24h, which decline by 48h after infection.  Macrophages do not significantly increase in S. pyogenes-infected NALT.  Intranasal infection of IFN-gamma -/- (GKO) C57BL/6 mice did not lead to systemic dissemination of wild type S. pyogenes, despite reduced expression of IFN-gamma-responsive mRNAs in NALT.   Infected GKO mice had an unregulated influx of neutrophils into NALT compared to immunocompetant mice and mice treated with an anti-IFN-gamma antibody more rapidly cleared S. pyogenes from NALT.  Thus, IFN-gamma-induced responses have a suppressive influence on early clearance of this pathogen from NALT."'
GSE11496_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We use array analysis to determine the global mRNA shift into polysomes following a stress response, and to compare the translational response following activation of GCN2 versus PERK, two of the four eIF2alpha kinases."'
GSE11498_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Identification of novel monosodium urate crystal-induced mRNAs"'
GSE11498_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Objective. To identify novel monosodium urate (MSU) crystal-induced mRNAs by transcript profiling of isolated murine air pouch membranes."'
GSE11498_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Results. Eleven of the 12 most highly upregulated mRNAs related to innate immunity and inflammation. They included mRNAs encoding histidine decarboxylase (the enzyme that synthesizes histamine), interleukin (IL)-6, the cell surface receptors PUMA-g and TREM-1, and the polypeptides Irg1 and PROK-2. MSU crystals induced dramatic rises in these mRNAs in the pouch membrane within 3-8 hours after the surge in pro-inflammatory cytokine (IL-6, IL-1beta and TNFalpha) and immediate early gene (Egr-1) transcription, which occurred 1h after crystal injection. MSU crystals induced these mRNAs in cultured macrophages with similar kinetics but lower fold changes. In keeping with their downregulation by MSU crystals according to the microarrays, qPCR confirmed that TREM-2 and granzyme D mRNAs decreased 79% and 94%, respectively, in MSU crystal inflamed membranes."'
GSE11507_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Background. Abcb4 (-/-) mice secrete phosphatidylcholine-deficient bile and develop sclerosing cholangitis (SC). The cholangitis involves differential hepatic transcription of genes whose products govern inflammation, activation of hepatic stellate cells and fibrosis.  This study was undertaken to test the hypothesis that several genes involved in regulation of tissue inflammation and fibrosis display transcription rates that reflect SC disease activity. Methods. Abcb4 (-/-) mice fed cholic acid (CA) display high SC activity and ursodeoxycholic acid (UDCA) fed mice display low SC activity. Differential hepatic transcription of genes was accordingly measured in abcb4 (-/-) mice maintained on CA- and UDCA-supplemented diets using cDNA microarrays. Abcb4 (+/+) mice served as controls. The differential transcription of selected genes was verified by real time polymerase chain reaction. Liver tissue pathology was quantified by histopathology scoring and immunohistochemistry to visualize bile duct cells and activated hepatic stellate cells. Results. Differential transcription of  Ccl2, Ccl20, Cxcl10, Nfκb1, Nfκb2, Tgfβ1, Tgfβ2, Sparc, Ctgf, Lgals3, Elf3, Spp1, Pdgfa, Pdgfrb, Col1a1, Col1a2 and Col4a1 genes paralleled the differing SC activities of cholic acid- and UDCA-fed abcb4 (-/-) mice. Histopathology scores and immunohistochemistry showed greatly enhanced activation of hepatic stellate cells during high SC activity due to CA feeding. Conclusion. Differential transcription of several genes relating to tissue inflammation and hepatic stellate cell activation parallels SC activity in abcb4 (-/-) mice. Data on their differential transcription may be used to gauge SC disease activity. "'
GSE11523_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Biologists rely on morphology, function, and specific markers to define the differentiation status of cells. Transcript profiling has expanded the repertoire of these markers by providing the snapshot of cellular status that reflects the activity of all genes. However, such data have been used only to assess relative similarities and differences of these cells. Here we show that principal component analysis (PCA) of global gene expression profiles map cells in multidimensional transcript profile space and the positions of differentiating cells progress in a stepwise manner along trajectories starting from undifferentiated embryonic stem (ES) cells located in the apex. We present three cell lineage trajectories, which represent the differentiation of ES cells into the first three lineages in mammalian development: primitive endoderm, trophoblast, and primitive ectoderm/neural ectoderm. The positions of the cells along these trajectories seem to reflect the developmental potency of cells and can be used as a scale for the potential of cells. Indeed, we show that embryonic germ (EG) cells and induced pluripotent (iPS) cells are mapped near the origin of the trajectories, whereas mouse embryo fibroblast (MEF) and fibroblast cell lines are mapped near the far end of the trajectories. We propose that this method can be used as the non-operational semi-quantitative definition of cell differentiation status and developmental potency. Furthermore, the global expression profiles of cell lineages provide a framework for the future study of in vitro and in vivo cell differentiation."'
GSE11533_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The basic helix-loop-helix transcriptional repressor twist1, as an antagonist of nuclear factor κB (NF-κB)-dependent cytokine expression, is involved in the regulation of inflammation-induced immunopathology. We could show that twist1 is expressed by activated T helper (Th) 1 effector memory cells. Induction of twist1 in Th cells is dependent on NF-κB, nuclear factor of activated T cells (NFAT), and interleukin (IL)-12 signaling via signal transducer and activator of transcription (STAT) 4. Expression of twist1 is transient following T-cell receptor engagement, and increases upon repeated stimulation of Th1 cells. Imprinting for enhanced twist1 expression is characteristic of repeatedly restimulated effector memory Th cells and thus of the pathogenic memory Th cells of chronic inflammation. Th lymphocytes from the inflamed joint or gut tissue of patients with rheumatic diseases, Crohn’s disease or ulcerative colitis express high levels of twist1. Expression of twist1 in Th1 lymphocytes limits the expression of the cytokines interferon-γ, IL-2 and tumor necrosis factor-α, and ameliorates Th1-mediated immunopathology in delayed-type hypersensitivity and antigen-induced arthritis. In order to identify the effect of twist1 expression on the function of Th cells, twist1 was ectopically expressed and the transcriptome was compared to empty-virus infected control cells. In addition, this experiment allows for the identification of genes regulated by the transcription factor twist1."'
GSE11533_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_overall_design	"Genes differentially expressed upon ectopic twist1 overexpression. Splenic DO11.10 cells were activated in vitro with the cognate peptide ova327-339 in the presence of 1ng/ml IL-12 and 1ng/ml IL-2. On day 2 cells were infected with control virus, or twist1-encoding virus. On day 5 cells were sorted according to expression of the viral marker gene gfp. Cells were restimulated for four hours with PMA/ionomycin. The transcriptional profiles of duplicates of cultures were compared using Affymetrix Murine Genome (MG) 430A 2.0 GeneChip arrays. "'
GSE11534_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Upon activation under appropriate costimulatory conditions, naive T helper (Th) cells differentiate into Th2 or Th17 cells, each characterized by the expression of specific effector cytokines. In response to a repeated stimulation with antigen, Th cells develop a stable memory for the expression of those cytokines as well as for other secreted or membrane-associated factors. The stable memory for the expression of proinflammatory effector functions may explain the resistance of Th effector cells to conventional immunosuppressive therapy, and the inability of immunosuppression to cure chronic inflammation. The imprinting of the functional memory is based on epigenetic modifications and expression of distinct transcription factors. In this project, we compare the transcriptomes of once and repeatedly activated murine Th1 cells, to identify genes that induce and maintain the functional memory and control the persistence of pathogenic memory Th1 cells. This in turn might help to discriminate pathogenic versus protective cells in immunopathology and present novel targets for the diagnosis and therapy of chronic inflammatory disease. "'
GSE11534_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Genes differentially expressed in once versus four times stimulated Th1 cells. In vitro polarization of murine naïve DO11.10 T cells towards Th1 direction (5 ng/ml recombinant murine IL-12, 5 μg/ml anti-IL-4 antibody) with antigenic stimulation (ova323-339 and irradiated splenic APCs). The transcriptional profiles of resting one week old Th1 (Th1 1w) cells and resting 4 week old Th1 (Th1 4w) cells were compared using Affymetrix Murine Genome (MG) U74V2A GeneChip arrays."'
GSE11547_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"After day 8.5 mouse embryos from p53 heterozygous crosses were treated in either control (38C) water bath or hot (43C) water bath for 10 minutes, they were collected, genotyped, and embryos of similar genotype (+/+; +/-; -/-) and treatment were pooled. Total RNA of biological quarduplicate samples were isolated each from p53 +/+, +/-, -/- embryos. Total RNA of each sample was obtained from 3-7 embryos. Gene expression differences between the three genotypes were examined."'
GSE11557_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Lineage(-), Sca-1(+), c-Kit(+) cells derived from Evi-1(flox/flox) mice were transduced with GFP or Cre-GFP expressing retroviruses. GFP(+) cells were sorted and  and analyzed by Affymetrix® Mouse Genome 430 2.0 Array® for gene expression. Two independent experiments were performed."'
GSE11572_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"The following constructs were used:  Mus musculus  Klf4 full length, (ref|NM_010637.1) cDNA, Mus musculus cyclin-dependent kinase inhibitor 1A (P21) (Cdkn1a), cDNA (ref|NM_007669.3) were fused in frame to the modified oestrogen receptor ERT2 (Feil et al., 1997) and cloned into a retroviral vector (Mieg3) expressing the constructs together with eGFP after an internal ribosomal entry site . (Williams et al., 2000). For Klf4, a mutant comprinsing the zinc- finger domains only  AA 393 – 474 (Klf4 dN) as well as a mutant comprising the entire protein except the zinc fingers AA 1-393 (Klf4-dC) were constructed and fused in frame to the modified oestrogen receptor."'
GSE11572_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"BM cells from 5-FU treated mice were infected with viral constructs, sorted for GFP expression (day8), plated in IMDM , 10% FCS, 2mM Gln, 1% P/S, supplemented with 50ng/ml rSCF, 100ng/ml TPO and 100ng/ml G-CSF and cultured for 72h (day8-day10). On day10 cells were stimulated with 4-OHT (1uM) for 16h. After that time, total RNA was isolated by Trizol method."'
GSE11572_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"BM cells from 5-FU treated mice were infected with viral constructs, sorted for GFP expression (day8), plated in IMDM , 10% FCS, 2mM Gln, 1% P/S, supplemented with 50ng/ml rSCF, 100ng/ml TPO and 100ng/ml G-CSF and cultured for 72h (day8-day10). On day10 cells were stimulated with 4-OHT (1uM) for 16h. After that time, total RNA was isolated by Trizol method."'
GSE11576-GPL5811_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RNA mapping and ChIP with tiling arrays in FGF-stimulated NIH3T3 cells"'
GSE11576-GPL5811_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Transcription initiation in mammals is assumed to be independently controlled among nearby genes. On the other hand, recent large-scale transcriptome analyses have shown that the genome is pervasively transcribed, such that the majority of its DNA gives rise to RNAs. A simple question therefore arises: is it possible to pinpoint and activate a particular locus without perturbing numerous neighboring transcripts? Here we show that intensive transcription of immediate-early genes (IEGs) in response to growth factor stimulation is often accompanied by co-upregulation of their neighboring genes. Profiling primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centered on IEGs. Even in surrounding intergenic regions, which lack annotated protein-coding genes, transcriptional upregulation took place at the same time. We further found that acetylation levels of histone H3 and H4 are elevated along with the IEG induction and neighbouring co-upregulation, and that inhibition of the mitogen-activated protein kinase (MAPK) pathway or the transcription factor SRF suppresses all these transcriptional upregulation. These results suggest that transcriptional activation has a ripple effect, and causes a substantial fluctuation in multiple intragenic and intergenic transcripts."'
GSE11576-GPL5811_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The following RNA mapping and ChIP experiments were performed using tiling arrays in FGF-stimulated NIH3T3 cells.  1) Expression time course of nuclear RNA  2) Expression time course of total RNA  3) Effect of the MEK inhibitor U0126  4) ChIP-chip with anti-acetylated histone H3 antibody  5) ChIP-chip with anti-SRF antibody"'
GSE11576-GPL6444_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RNA mapping and ChIP with tiling arrays in FGF-stimulated NIH3T3 cells"'
GSE11576-GPL6444_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Transcription initiation in mammals is assumed to be independently controlled among nearby genes. On the other hand, recent large-scale transcriptome analyses have shown that the genome is pervasively transcribed, such that the majority of its DNA gives rise to RNAs. A simple question therefore arises: is it possible to pinpoint and activate a particular locus without perturbing numerous neighboring transcripts? Here we show that intensive transcription of immediate-early genes (IEGs) in response to growth factor stimulation is often accompanied by co-upregulation of their neighboring genes. Profiling primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centered on IEGs. Even in surrounding intergenic regions, which lack annotated protein-coding genes, transcriptional upregulation took place at the same time. We further found that acetylation levels of histone H3 and H4 are elevated along with the IEG induction and neighbouring co-upregulation, and that inhibition of the mitogen-activated protein kinase (MAPK) pathway or the transcription factor SRF suppresses all these transcriptional upregulation. These results suggest that transcriptional activation has a ripple effect, and causes a substantial fluctuation in multiple intragenic and intergenic transcripts."'
GSE11576-GPL6444_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The following RNA mapping and ChIP experiments were performed using tiling arrays in FGF-stimulated NIH3T3 cells.  1) Expression time course of nuclear RNA  2) Expression time course of total RNA  3) Effect of the MEK inhibitor U0126  4) ChIP-chip with anti-acetylated histone H3 antibody  5) ChIP-chip with anti-SRF antibody"'
GSE11576-GPL6445_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RNA mapping and ChIP with tiling arrays in FGF-stimulated NIH3T3 cells"'
GSE11576-GPL6445_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Transcription initiation in mammals is assumed to be independently controlled among nearby genes. On the other hand, recent large-scale transcriptome analyses have shown that the genome is pervasively transcribed, such that the majority of its DNA gives rise to RNAs. A simple question therefore arises: is it possible to pinpoint and activate a particular locus without perturbing numerous neighboring transcripts? Here we show that intensive transcription of immediate-early genes (IEGs) in response to growth factor stimulation is often accompanied by co-upregulation of their neighboring genes. Profiling primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centered on IEGs. Even in surrounding intergenic regions, which lack annotated protein-coding genes, transcriptional upregulation took place at the same time. We further found that acetylation levels of histone H3 and H4 are elevated along with the IEG induction and neighbouring co-upregulation, and that inhibition of the mitogen-activated protein kinase (MAPK) pathway or the transcription factor SRF suppresses all these transcriptional upregulation. These results suggest that transcriptional activation has a ripple effect, and causes a substantial fluctuation in multiple intragenic and intergenic transcripts."'
GSE11576-GPL6445_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The following RNA mapping and ChIP experiments were performed using tiling arrays in FGF-stimulated NIH3T3 cells.  1) Expression time course of nuclear RNA  2) Expression time course of total RNA  3) Effect of the MEK inhibitor U0126  4) ChIP-chip with anti-acetylated histone H3 antibody  5) ChIP-chip with anti-SRF antibody"'
GSE11576-GPL6446_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RNA mapping and ChIP with tiling arrays in FGF-stimulated NIH3T3 cells"'
GSE11576-GPL6446_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Transcription initiation in mammals is assumed to be independently controlled among nearby genes. On the other hand, recent large-scale transcriptome analyses have shown that the genome is pervasively transcribed, such that the majority of its DNA gives rise to RNAs. A simple question therefore arises: is it possible to pinpoint and activate a particular locus without perturbing numerous neighboring transcripts? Here we show that intensive transcription of immediate-early genes (IEGs) in response to growth factor stimulation is often accompanied by co-upregulation of their neighboring genes. Profiling primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centered on IEGs. Even in surrounding intergenic regions, which lack annotated protein-coding genes, transcriptional upregulation took place at the same time. We further found that acetylation levels of histone H3 and H4 are elevated along with the IEG induction and neighbouring co-upregulation, and that inhibition of the mitogen-activated protein kinase (MAPK) pathway or the transcription factor SRF suppresses all these transcriptional upregulation. These results suggest that transcriptional activation has a ripple effect, and causes a substantial fluctuation in multiple intragenic and intergenic transcripts."'
GSE11576-GPL6446_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The following RNA mapping and ChIP experiments were performed using tiling arrays in FGF-stimulated NIH3T3 cells.  1) Expression time course of nuclear RNA  2) Expression time course of total RNA  3) Effect of the MEK inhibitor U0126  4) ChIP-chip with anti-acetylated histone H3 antibody  5) ChIP-chip with anti-SRF antibody"'
GSE11576-GPL6447_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RNA mapping and ChIP with tiling arrays in FGF-stimulated NIH3T3 cells"'
GSE11576-GPL6447_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Transcription initiation in mammals is assumed to be independently controlled among nearby genes. On the other hand, recent large-scale transcriptome analyses have shown that the genome is pervasively transcribed, such that the majority of its DNA gives rise to RNAs. A simple question therefore arises: is it possible to pinpoint and activate a particular locus without perturbing numerous neighboring transcripts? Here we show that intensive transcription of immediate-early genes (IEGs) in response to growth factor stimulation is often accompanied by co-upregulation of their neighboring genes. Profiling primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centered on IEGs. Even in surrounding intergenic regions, which lack annotated protein-coding genes, transcriptional upregulation took place at the same time. We further found that acetylation levels of histone H3 and H4 are elevated along with the IEG induction and neighbouring co-upregulation, and that inhibition of the mitogen-activated protein kinase (MAPK) pathway or the transcription factor SRF suppresses all these transcriptional upregulation. These results suggest that transcriptional activation has a ripple effect, and causes a substantial fluctuation in multiple intragenic and intergenic transcripts."'
GSE11576-GPL6447_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The following RNA mapping and ChIP experiments were performed using tiling arrays in FGF-stimulated NIH3T3 cells.  1) Expression time course of nuclear RNA  2) Expression time course of total RNA  3) Effect of the MEK inhibitor U0126  4) ChIP-chip with anti-acetylated histone H3 antibody  5) ChIP-chip with anti-SRF antibody"'
GSE11576-GPL6448_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RNA mapping and ChIP with tiling arrays in FGF-stimulated NIH3T3 cells"'
GSE11576-GPL6448_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Transcription initiation in mammals is assumed to be independently controlled among nearby genes. On the other hand, recent large-scale transcriptome analyses have shown that the genome is pervasively transcribed, such that the majority of its DNA gives rise to RNAs. A simple question therefore arises: is it possible to pinpoint and activate a particular locus without perturbing numerous neighboring transcripts? Here we show that intensive transcription of immediate-early genes (IEGs) in response to growth factor stimulation is often accompanied by co-upregulation of their neighboring genes. Profiling primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centered on IEGs. Even in surrounding intergenic regions, which lack annotated protein-coding genes, transcriptional upregulation took place at the same time. We further found that acetylation levels of histone H3 and H4 are elevated along with the IEG induction and neighbouring co-upregulation, and that inhibition of the mitogen-activated protein kinase (MAPK) pathway or the transcription factor SRF suppresses all these transcriptional upregulation. These results suggest that transcriptional activation has a ripple effect, and causes a substantial fluctuation in multiple intragenic and intergenic transcripts."'
GSE11576-GPL6448_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The following RNA mapping and ChIP experiments were performed using tiling arrays in FGF-stimulated NIH3T3 cells.  1) Expression time course of nuclear RNA  2) Expression time course of total RNA  3) Effect of the MEK inhibitor U0126  4) ChIP-chip with anti-acetylated histone H3 antibody  5) ChIP-chip with anti-SRF antibody"'
GSE11576-GPL6449_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RNA mapping and ChIP with tiling arrays in FGF-stimulated NIH3T3 cells"'
GSE11576-GPL6449_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Transcription initiation in mammals is assumed to be independently controlled among nearby genes. On the other hand, recent large-scale transcriptome analyses have shown that the genome is pervasively transcribed, such that the majority of its DNA gives rise to RNAs. A simple question therefore arises: is it possible to pinpoint and activate a particular locus without perturbing numerous neighboring transcripts? Here we show that intensive transcription of immediate-early genes (IEGs) in response to growth factor stimulation is often accompanied by co-upregulation of their neighboring genes. Profiling primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centered on IEGs. Even in surrounding intergenic regions, which lack annotated protein-coding genes, transcriptional upregulation took place at the same time. We further found that acetylation levels of histone H3 and H4 are elevated along with the IEG induction and neighbouring co-upregulation, and that inhibition of the mitogen-activated protein kinase (MAPK) pathway or the transcription factor SRF suppresses all these transcriptional upregulation. These results suggest that transcriptional activation has a ripple effect, and causes a substantial fluctuation in multiple intragenic and intergenic transcripts."'
GSE11576-GPL6449_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The following RNA mapping and ChIP experiments were performed using tiling arrays in FGF-stimulated NIH3T3 cells.  1) Expression time course of nuclear RNA  2) Expression time course of total RNA  3) Effect of the MEK inhibitor U0126  4) ChIP-chip with anti-acetylated histone H3 antibody  5) ChIP-chip with anti-SRF antibody"'
GSE11576-GPL6450_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RNA mapping and ChIP with tiling arrays in FGF-stimulated NIH3T3 cells"'
GSE11576-GPL6450_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Transcription initiation in mammals is assumed to be independently controlled among nearby genes. On the other hand, recent large-scale transcriptome analyses have shown that the genome is pervasively transcribed, such that the majority of its DNA gives rise to RNAs. A simple question therefore arises: is it possible to pinpoint and activate a particular locus without perturbing numerous neighboring transcripts? Here we show that intensive transcription of immediate-early genes (IEGs) in response to growth factor stimulation is often accompanied by co-upregulation of their neighboring genes. Profiling primary transcripts in the nucleus with whole-genome tiling arrays delineated simultaneous activation of transcription centered on IEGs. Even in surrounding intergenic regions, which lack annotated protein-coding genes, transcriptional upregulation took place at the same time. We further found that acetylation levels of histone H3 and H4 are elevated along with the IEG induction and neighbouring co-upregulation, and that inhibition of the mitogen-activated protein kinase (MAPK) pathway or the transcription factor SRF suppresses all these transcriptional upregulation. These results suggest that transcriptional activation has a ripple effect, and causes a substantial fluctuation in multiple intragenic and intergenic transcripts."'
GSE11576-GPL6450_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The following RNA mapping and ChIP experiments were performed using tiling arrays in FGF-stimulated NIH3T3 cells.  1) Expression time course of nuclear RNA  2) Expression time course of total RNA  3) Effect of the MEK inhibitor U0126  4) ChIP-chip with anti-acetylated histone H3 antibody  5) ChIP-chip with anti-SRF antibody"'
GSE11585_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Granulosa cell gene expression in gonadotropin-treated ERbeta-het and ERbeta-null mice"'
GSE11585_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The aim of this study was to determine the role of ERβ in the response of mouse granulosa cells to PMSG (an FSH analog) by comparing the gene expression profiles of ERβ-het and ERβ-null animals treated with this compound."'
GSE11585_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"ERβ-het and ERβ-null mice were treated with PMSG for 48h and granulosa cells isolated and pooled according to gentoype, resulting in the production of two RNA samples (one biological replicate per gentoype). There were two hyb replicates for the comparison. Two slides were hybridized for the sample pairing to allow for dye reversals (technical replicates)."'
GSE11586_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"Processing of Immunoglobulin heavy chain (IgH) mRNA is a paradigm for competition between splicing and polyadenylation.  In plasma cells pre-mRNA is polyadenylated mainly at the promoter-proximal secretory site while B-cells utilize a cryptic 5’ splice site in the last secretory-specific exon; these are mutually exclusive events for all IgH pre-mRNAs.  Transcription elongation factor ELL2, more abundant in plasma cells relative to B-cells, was down-modulated by overexpression of heterogenous ribonucleoprotein F, a condition which reduced production of secretory IgH mRNA.  Transfection of B-cells with ELL2 and the IgH reporter showed an accelerated use of the secretory poly(A) site, positioned in competition with the splice to M1; a small interfering RNA to ELL2 reduced expression of IgH secretory mRNA.  Co-transcription factors ELL1 and PC4 were ineffective at driving secretory-poly(A) site use.  ELL2 had little effect on poly(A) site choice with reporters containing tandem-linked poly(A) sites.  Shorter forms of ELL2 protein result from both internal initiation at M186 and protein processing.  An alternative splicing reporter driven by IgH or non-Ig promoters revealed that ELL2 and its M186 initiated form were able to accelerate exon skipping.  Therefore, ELL2 influences IgH pre-mRNA processing through facilitating skipping of the alternative splice to the membrane form."'
GSE11586_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_overall_design	"AxJ plasma cells were stably transfected to overexpress hnRNP-F, -H or empty vector. Clones showing high overexpression levels of F or H by western blot were selected. The IgH sec to mb ratios of these clones were determined. A global gene expression analysis was performed on mRNA from two clones from hnRNP-F, which demonstrated a lower sec:mb ratio, and one from each of the controls: overexpression of hnRNP-H, or transfection with empty vector, or A20 B-cells, using Affymetrix gene micro array technology."'
GSE11628_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The molecular processes underlying the properties of ESC are yet unknown even when it's well established that LIF/STAT3 is neccesary for the maintenance of pluripotency. Other pathways as Wnt are may be implicated in the regulation of the biological mechanisms in mESC. Work model: D3-ES cultivated with or without LIF and treated with chronic (7 days) low doses (50nM) of GSK3 β inhibitor (lithium)."'
GSE11629_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"This study uses microarray analysis to examine the fate of multiple C-ion-irradiated tumors in vivo to gain a comprehensive overview of the changes in gene expression induced by C-ion irradiation. Four murine tumors were irradiated in vivo with C-ions at a single dose, and gamma-rays were used as a reference beam."'
GSE11660_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Bone marrow stromal cells (BMSCs) are multipotent stem cells that preferentially differentiate into mesenchymal cells. If they can be dedifferentiated into embryonic stem cell-like cells, they will be a highly attractive source for cell therapy. Cell and egg extracts have been used in a few studies to evaluate nuclear reprogramming, but these have not examined cell pluripotency in any detail. In this study, we used a cell reversible permeabilization method to treat BMSC with Xenopus laevis mitotic egg extract. We observed an upregulation of the pluripotent protein Oct3/4 in BMSCs treated by this extract. We also further evaluated transcriptional changes with a focused stem cell oligonucleotide array. A number of genes involved in the Notch or Wnt signaling pathways were upregulated in BMSC exposed to Xenopus egg extract. In conclusion, our microarray data from BMSCs exposure to egg extracts may provide interesting clues regarding factors involved in nuclear reprogramming. Our approach is an alternative method towards dedifferentiation of cells without genetic modification, which is preferable in the clinical situation."'
GSE11660_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Bone marrow stromal cells (BMSCs) are multipotent stem cells that preferentially differentiate into mesenchymal cells. If they can be dedifferentiated into embryonic stem cell-like cells, they will be a highly attractive source for cell therapy. Cell and egg extracts have been used in a few studies to evaluate nuclear reprogramming, but these have not examined cell pluripotency in any detail. In this study, we used a cell reversible permeabilization method to treat BMSC with Xenopus laevis mitotic egg extract. We observed an upregulation of the pluripotent protein Oct3/4 in BMSCs treated by this extract. We also further evaluated transcriptional changes with a focused stem cell oligonucleotide array. A number of genes involved in the Notch or Wnt signaling pathways were upregulated in BMSC exposed to Xenopus egg extract. In conclusion, our microarray data from BMSCs exposure to egg extracts may provide interesting clues regarding factors involved in nuclear reprogramming. Our approach is an alternative method towards dedifferentiation of cells without genetic modification, which is preferable in the clinical situation."'
GSE11661_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Muscle ring finger-1 (MuRF1) is a muscle-specific protein implicated in the regulation of cardiac myocyte size and contractility. MuRF2, a closely related family member, redundantly interacts with protein substrates, and hetero-dimerizes with MuRF1. Mice lacking either MuRF1 or MuRF2 are phenotypically normal whereas mice lacking both proteins develop a spontaneous cardiac and skeletal muscle hypertrophy indicating cooperative control of muscle mass by MuRF1 and MuRF2. In order to identify the role that MuRF1 plays in regulating cardiac hypertrophy in vivo, we created transgenic mice expressing increased amounts of cardiac MuRF1. Adult MuRF1 transgenic (Tg+) hearts exhibited a non-progressive thinning of the left ventricular wall and a concomitant decrease in cardiac function. Experimental induction of cardiac hypertrophy by trans-aortic constriction (TAC) induced rapid failure of MuRF1 Tg+ hearts. Microarray analysis identified that the levels of genes associated with metabolism (and in particular mitochondrial processes) were significantly altered in MuRF1 Tg+ hearts, both at baseline and during the development of cardiac hypertrophy. Surprisingly, ATP levels in MuRF1 Tg+ mice did not differ from wild type mice despite the depressed contractility following TAC. To explain this discrepancy between the ongoing heart failure and maintained ATP levels in MuRF1 Tg+ hearts, we compared the level and activity of creatine kinase (CK) between wild type and MuRF1 Tg+ hearts. Although mCK and CK-M/B protein levels were unaffected in MuRF1 Tg+ hearts, total CK activity was significantly inhibited. We conclude that MuRF1’s inhibition of CK activity leads to increased susceptibility to heart failure following TAC, demonstrating for the first time that MuRF1 regulates cardiac energetics in vivo."'
GSE11661_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Muscle ring finger-1 (MuRF1) is a muscle-specific protein implicated in the regulation of cardiac myocyte size and contractility. MuRF2, a closely related family member, redundantly interacts with protein substrates, and hetero-dimerizes with MuRF1. Mice lacking either MuRF1 or MuRF2 are phenotypically normal whereas mice lacking both proteins develop a spontaneous cardiac and skeletal muscle hypertrophy indicating cooperative control of muscle mass by MuRF1 and MuRF2. In order to identify the role that MuRF1 plays in regulating cardiac hypertrophy in vivo, we created transgenic mice expressing increased amounts of cardiac MuRF1. Adult MuRF1 transgenic (Tg+) hearts exhibited a non-progressive thinning of the left ventricular wall and a concomitant decrease in cardiac function. Experimental induction of cardiac hypertrophy by trans-aortic constriction (TAC) induced rapid failure of MuRF1 Tg+ hearts. Microarray analysis identified that the levels of genes associated with metabolism (and in particular mitochondrial processes) were significantly altered in MuRF1 Tg+ hearts, both at baseline and during the development of cardiac hypertrophy. Surprisingly, ATP levels in MuRF1 Tg+ mice did not differ from wild type mice despite the depressed contractility following TAC. To explain this discrepancy between the ongoing heart failure and maintained ATP levels in MuRF1 Tg+ hearts, we compared the level and activity of creatine kinase (CK) between wild type and MuRF1 Tg+ hearts. Although mCK and CK-M/B protein levels were unaffected in MuRF1 Tg+ hearts, total CK activity was significantly inhibited. We conclude that MuRF1’s inhibition of CK activity leads to increased susceptibility to heart failure following TAC, demonstrating for the first time that MuRF1 regulates cardiac energetics in vivo."'
GSE11661_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Three-condition experiment, MuRF1 Tg+ vs. WT mice. Biological replicates: 4 WT baseline, 3 MuRF1 Tg+ baseline, cardiac overpressure hypertrophy induced by trans-aortic banding at 1 week (3 WT, 3 MurF Tg) and 4 weeks (3 WT, 3 MurF Tg), hearts harvested. One replicate per array."'
GSE11662_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"GADD45a in ventilator-induced lung injury: role of Akt signaling"'
GSE11662_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We explored the mechanistic involvement of the growth arrest and DNA damageinducible gene, GADD45a, in LPS- and ventilator-induced inflammatory lung injury (VILI). Multiple biochemical and genomic parameters of inflammatory lung injury indicated GADD45a-/- mice to be modestly susceptible to intratracheal LPS-induced lung injury and profoundly susceptible to high tidal volume ventilation-induced lung injury (VILI) with increases in microvascular permeability and levels of inflammatory cytokines in bronchoalveolar lavage. Expression profiling of lung tissues from GADD45a-/- mice revealed strong dysregulation in the B cell receptor signaling pathway suggesting involvement of PI3 kinase/Akt signaling components while the wild type controls depicted no observable changes. Western blot analyses of lung homogenates confirmed ~50% reduction in Akt protein levels in GADD45a-/- mice accompanied by marked increases in Akt ubiquitination. Electrical resistance measurements across human lung endothelial cell monolayers with either reduced GADD45a or Akt expression (siRNAs) revealed significant potentiation of LPS-induced human lung endothelial barrier dysfunction which was attenuated by overexpression of a constitutively active Akt1 transgene. These studies validate GADD45a as a novel candidate gene in inflammatory lung injury and a significant participant in vascular barrier regulation via effects on Akt-mediated endothelial signaling"'
GSE11662_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"We explored the mechanistic involvement of the growth arrest and DNA damageinducible gene, GADD45a, in LPS- and ventilator-induced inflammatory lung injury (VILI). Multiple biochemical and genomic parameters of inflammatory lung injury indicated GADD45a-/- mice to be modestly susceptible to intratracheal LPS-induced lung injury and profoundly susceptible to high tidal volume ventilation-induced lung injury (VILI) with increases in microvascular permeability and levels of inflammatory cytokines in bronchoalveolar lavage. Expression profiling of lung tissues from GADD45a-/- mice revealed strong dysregulation in the B cell receptor signaling pathway suggesting involvement of PI3 kinase/Akt signaling components while the wild type controls depicted no observable changes. Western blot analyses of lung homogenates confirmed ~50% reduction in Akt protein levels in GADD45a-/- mice accompanied by marked increases in Akt ubiquitination. Electrical resistance measurements across human lung endothelial cell monolayers with either reduced GADD45a or Akt expression (siRNAs) revealed significant potentiation of LPS-induced human lung endothelial barrier dysfunction which was attenuated by overexpression of a constitutively active Akt1 transgene. These studies validate GADD45a as a novel candidate gene in inflammatory lung injury and a significant participant in vascular barrier regulation via effects on Akt-mediated endothelial signaling"'
GSE11674-GPL81_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed."'
GSE11674-GPL82_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed."'
GSE11679_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Balb c/J offspring were briefly separated from mothers for 15 minutes each morning on postnatal days 1-14 (handled group) or left undisturbed.  At 8 weeks of age mice were tested in the open-field and light-dark behavioral paradigms to verify a handling-induced behavioral phenotype.  2 weeks after behavioral testing, animals were sacrificed and the CA1 region was microdissected.  CA1 regions were stored at -20C in RNA later.  RNA was extracted from 8 samples (4 handled and 4 non-handled) using Trizol.  RNA was extracted from second group of animals (7 handled and 10 non-handled) using Qiagen RNA/DNA columns.  All total RNA samples were double round amplied and labeled using standard Affymetrix protocols and hybridized to Mouse 430_2.0 arrays in parallel."'
GSE11680_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Balb c/J offspring were briefly separated from mothers for 15 minutes each morning on postnatal days 1-14 (handled group) or left undisturbed.  At 8 weeks of age mice were tested in the open-field and light-dark behavioral paradigms to verify a handling-induced behavioral phenotype.  2 weeks after behavioral testing, animals were sacrificed and the CA1 region was microdissected.  CA1 regions were stored at -20C in RNA later.  RNA was extracted from 8 samples (4 handled and 4 non-handled) using Trizol.  RNA was extracted from second group of animals (7 handled and 10 non-handled) using Qiagen RNA/DNA columns.  All total RNA samples were double round amplied and labeled using standard Affymetrix protocols and hybridized to Mouse 430_2.0 arrays in parallel."'
GSE11684_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We use array analysis to determine the global mRNA shift into polysomes following a stress response, and to compare the translational response following activation of GCN2 versus PERK, two of the four eIF2alpha kinases."'
GSE11685_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"Translational response following activation of GCN2 versus PERK"'
GSE11685_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We use array analysis to determine the global mRNA shift into polysomes following a stress response, and to compare the translational response following activation of GCN2 versus PERK, two of the four eIF2alpha kinases."'
GSE11687_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The Ca2+ oscillations initiated by the fertilizing sperm (but terminating concomitant with pronucleus formation) apparently ensure that the events constituting egg activation occur in the correct temporal order; early events (e.g., cortical granule exocytosis) require fewer oscillations than later events (e.g., recruitment of maternal mRNA). Whether the Ca2+ signaling events impact long-term development, in particular development to term, is unknown. Using fertilized eggs that have undergone the first few Ca2+ oscillations, we developed procedures that result either in inhibiting or stimulating the natural pattern of Ca2+ signaling of inseminated eggs. Although the incidence of development to the blastocyst stage is unaltered by these procedures, fewer offspring are born following embryo transfer, indicating that developmental competence of the blastocysts is reduced. Interestingly, embryo transfer experiments reveal that when the natural regime of Ca2+ oscillations is precociously interrupted, the incidence of implantation is compromised whereas hyper-stimulation of Ca2+ signaling events compromises post-implantation development. Moreover, although there was no major difference in the overall growth rates of the offspring, those obtained following hyper-stimulation exhibited a far greater variability in their weight. Analysis of global patterns of gene expression by microarray analysis revealed that approximately 20% of the transcripts are mis-regulated when too few oscillations are experienced by the embryo and EASE analysis indicates that genes preferentially involved in RNA processing and polymerase II transcription are differentially affected. In addition, a set of genes involved in cell adhesion is also mis-expressed and could thus be mechanistically linked to the observed reduced implantation. Only about 3% of the transcripts were mis-regulated following hyper-stimulation, and EASE analysis indicates that genes preferentially involved in metabolism are differentially affected. In toto, these results indicate that a range Ca2+ signaling events following fertilization (an excess or reduction) has long-term effects on both gene expression and development to term."'
GSE11702_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Gene expression profiling of a total of 3,774 genes in primary osteoblastic cells treated with TGF-beta1"'
GSE11702_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Primary osteoblasts cultured under serum-starved condition were treated or untreated with TGF-beta1 for 24 hr."'
GSE11719_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Comparison of gene expression induced in hearts excised from mice 24 or 48 hours after DMA or DMSO (vehicle) treatment."'
GSE11719_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"In isolated heart preparations, we observed that previous treatment with quinazoline DMA evoked both acute and late phases of cardioprotection. In this study, we adopted whole genome microarrays approach to investigate cardiac transcriptional responses induced in hearts from DMA treated mice in comparison to vehicle-only treatment."'
GSE11719_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In isolated heart preparations, we observed that previous treatment with quinazoline DMA evoked both acute and late phases of cardioprotection. In this study, we adopted whole genome microarrays approach to investigate cardiac transcriptional responses induced in hearts from DMA treated mice in comparison to vehicle-only treatment."'
GSE11723_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Expression data from hematopoietic stem cells plated on OP9 stroma expressing or not the Notch ligand Delta-like1. Results provide insight into the role of Notch signalling in megakaryocyte fate specification."'
GSE11726_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We analyzed whether cochlear removal-induced transcriptional changes in the cochlear nucleus (CN) were due to loss of electrical activity in the 8th nerve.  Pharmacological activity blockade of the auditory nerve for 24 h resulted in similar expression changes for only a subset of genes.  Thus, an additional factor not dependent on action potential-mediated signaling must also regulate transcriptional responses to deafferentation in the CN.  "'
GSE11727_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Dlx3 over-expression in mouse embryonic fibroblasts changed the expression level of numerous genes involved in osteogenesis and embryonic stem cell-related pathways as revealed by microarray analysis.  From the list of Dlx3 modulated genes we focused our attention on the study of two candidates, Lifr and Chrdl1.  Chromatin immunoprecipitation demonstrated the recruitment of Dlx3 transcription factor to the promoters of Lifr and Chrdl1, and luciferase assays confirmed the role of Dlx3 in the regulation of Lifr expression.  Over-expression of Dlx3 in mouse embryonic stem cells stimulated Lifr and Chrdl1 expression and inhibited expression of Id proteins and Bmp4.  We show that Dlx3 increases the expression of both soluble and transmembrane forms of Lifr.  Soluble Lifr may regulate extracellular Lif levels via solution binding, while transmembrane Lifr mediates the signal transduction pathway. The data suggests that Dlx3 may be involved in stem cell differentiation in a dosage dependent way through its interaction with Lifr and with Chrdl1, a known antagonist of Bmp4.  We speculate that Dlx3 may also be involved in osteoblast differentiation through interactions involving Lifr, Bmp, and Id proteins and signaling via the JAK/STAT and MAPK pathways.  In summary, our data suggests that Dlx3 proteins play a significant role in a highly tuned network in early embryogenesis."'
GSE11727_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Keywords: treated vs.untreated"'
GSE11732_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"Keywords: Comparative study of gene targets regulated by overexpression of the different Runx family members"'
GSE11732_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"6 samples (expression of different Runx family members); 5 in duplicate, 1 single.  2 control samples (empty vector) in duplicate. Cultures of Runx expressing cells were grown to confluence, treated with ethanol +/- 4OHT tamoxifen for 24 hours and harvested  for RNA extraction and hybridization on Affymetrix microarrays"'
GSE11732_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"6 samples (expression of different Runx family members); 5 in duplicate, 1 single.  2 control samples (empty vector) in duplicate. Cultures of Runx expressing cells were grown to confluence, treated with ethanol +/- 4OHT tamoxifen for 24 hours and harvested  for RNA extraction and hybridization on Affymetrix microarrays"'
GSE11766_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"Transcriptional repression of c-Myb and GATA-2 is involved in the effects of C/EBPα in p210 BCR/ABL-expressing cells"'
GSE11766_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Levels of C/EBPα are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis.  To assess the mechanisms involved in these effects, C/EBPα targets were identified  by microarray analyses.  Upon C/EBPα activation, expression of c-Myb and GATA-2 was  repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly   in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBPα was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBPα while c-Myb siRNA treatment enhanced C/EBPα-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic  differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBPα but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBPα induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBPα activation. In summary, the effects of C/EBPα in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2.  Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBPα appear to involve different transcription-regulated targets."'
GSE11766_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Levels of C/EBPα are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis.  To assess the mechanisms involved in these effects, C/EBPα targets were identified  by microarray analyses.  Upon C/EBPα activation, expression of c-Myb and GATA-2 was  repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly   in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBPα was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBPα while c-Myb siRNA treatment enhanced C/EBPα-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic  differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBPα but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBPα induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBPα activation. In summary, the effects of C/EBPα in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2.  Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBPα appear to involve different transcription-regulated targets."'
GSE11766_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Levels of C/EBPα are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis.  To assess the mechanisms involved in these effects, C/EBPα targets were identified  by microarray analyses.  Upon C/EBPα activation, expression of c-Myb and GATA-2 was  repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly   in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBPα was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBPα while c-Myb siRNA treatment enhanced C/EBPα-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic  differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBPα but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBPα induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBPα activation. In summary, the effects of C/EBPα in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2.  Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBPα appear to involve different transcription-regulated targets."'
GSE11766_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"48 samples total. 4-HT-treated 32D-BCR/ABL cells transduced with the MigRI empty vector, MigRI WT C/EBPα-ER , MigRI K298E C/EBPα-ER  (a DNA binding-deficient mutant) or MigRI-delta(177-191) C/EBPα-ER  (a mutant deficient in CDK2/CDK4 interaction). Total RNA was extracted at 0, 6, 9 and 12h post-4-HT treatment in triplicate and hybridized onto the Affymetrix MOE430 _2 array."'
GSE11770_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"In addition to lipid second messengers derived from the plasma membrane, increasing evidence supports the existence of nuclear lipid-dependent signaling networks. Diacylglycerol is a key second messenger, generated at the nuclear level, which is metabolized by diacylglycerol kinases (DGKs). It has been demonstrated that nuclear DGK-ζ negatively regulates cell cycle progression. The aim of this study was to identify key determinants of nuclear DGK-ζ-dependent cell cycle arrest in C2C12 mouse myoblasts. Using DNA microarrays, Real-Time RT-PCR and western blot, we demonstrated that nuclear DGK-ζ downregulated the expression of cyclin D1 and increased the expression of TIS21/BTG2/PC3, a transcriptional regulator of cyclin D1 with a strong anti-proliferative function. Overexpression of TIS21/BTG2/PC3 blocked the cells in G1 phase of the cell cycle and decreased the levels of Ser807/811 phosphorylated retinoblastoma protein, similarly to overexpression of DGK-ζ. Moreover, during myogenic differentiation of C2C12 cells, we showed an increase of TIS21/BTG2/PC3 expression and a decrease in cyclin D1 levels. siRNA downregulation of TIS21/BTG2/PC3 impaired myogenic differentiation by opposing cell cycle arrest. In summary, these data identify TIS21/BTG2/PC3 and cyclin D1 as downstream effectors of the nuclear DGK-ζ and highlight the importance of this DGK isoform in the regulation of myoblast proliferation and differentiation."'
GSE11770_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"single time point analysis of gene expression changes induced by DGK-zeta transfection in C2C12 cells. DGK-zeta-transfected cells are compared to untreated control cells and to EGFP-transfected cells."'
GSE11775_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"To identify candidate genes that might be related to the suppressive activity, the Treg cells expressing functional and mutant Foxp3 transcription factor were compared"'
GSE11790_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"These selected mice as well as NC mice were then treated with Rimonabant or Vehicle for 1 month. After treatment, mice were sacrificed and visceral and subcutaneous adipose tissues were collected and immediately frozen in liquid nitrogen."'
GSE11794-GPL81_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Untreated 32Dcl3 cell lines expressing oncogenic tyrosine kinases or cells treated with small molecule inhibitors"'
GSE11794-GPL81_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"Untreated 32Dcl3 cell lines expressing oncogenic tyrosine kinases or cells treated with small molecule inhibitors"'
GSE11794-GPL81_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"In our microarray study, we have total 22 samples from four different cell lines expressing BCR-ABL, TEL-ABL, FLT3-ITD or TEL-PDGF-betaR.  Each cell line was treated with specific small molecule inhibitors for 4 hours, then RNA was extracted and cRNA was hybridized to Affymetrix U74 oligonucleotide arrays. Untreated cells or cells treated with unrelated inhibitors were used as controls or references.  We have three replicates and six references obtained from three independent experiments for cells expressing BCR-ABL or FLT3-ITD.  We have one treated and one untreated sample for each cell line expressing TEL-ABL or TEL-PDGF-beta-R."'
GSE11794-GPL81_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"In our microarray study, we have total 22 samples from four different cell lines expressing BCR-ABL, TEL-ABL, FLT3-ITD or TEL-PDGF-betaR.  Each cell line was treated with specific small molecule inhibitors for 4 hours, then RNA was extracted and cRNA was hybridized to Affymetrix U74 oligonucleotide arrays. Untreated cells or cells treated with unrelated inhibitors were used as controls or references.  We have three replicates and six references obtained from three independent experiments for cells expressing BCR-ABL or FLT3-ITD.  We have one treated and one untreated sample for each cell line expressing TEL-ABL or TEL-PDGF-beta-R."'
GSE11794-GPL82_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Untreated 32Dcl3 cell lines expressing oncogenic tyrosine kinases or cells treated with small molecule inhibitors"'
GSE11794-GPL82_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"Untreated 32Dcl3 cell lines expressing oncogenic tyrosine kinases or cells treated with small molecule inhibitors"'
GSE11794-GPL82_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"In our microarray study, we have total 22 samples from four different cell lines expressing BCR-ABL, TEL-ABL, FLT3-ITD or TEL-PDGF-betaR.  Each cell line was treated with specific small molecule inhibitors for 4 hours, then RNA was extracted and cRNA was hybridized to Affymetrix U74 oligonucleotide arrays. Untreated cells or cells treated with unrelated inhibitors were used as controls or references.  We have three replicates and six references obtained from three independent experiments for cells expressing BCR-ABL or FLT3-ITD.  We have one treated and one untreated sample for each cell line expressing TEL-ABL or TEL-PDGF-beta-R."'
GSE11794-GPL82_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"In our microarray study, we have total 22 samples from four different cell lines expressing BCR-ABL, TEL-ABL, FLT3-ITD or TEL-PDGF-betaR.  Each cell line was treated with specific small molecule inhibitors for 4 hours, then RNA was extracted and cRNA was hybridized to Affymetrix U74 oligonucleotide arrays. Untreated cells or cells treated with unrelated inhibitors were used as controls or references.  We have three replicates and six references obtained from three independent experiments for cells expressing BCR-ABL or FLT3-ITD.  We have one treated and one untreated sample for each cell line expressing TEL-ABL or TEL-PDGF-beta-R."'
GSE11794-GPL83_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Untreated 32Dcl3 cell lines expressing oncogenic tyrosine kinases or cells treated with small molecule inhibitors"'
GSE11794-GPL83_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"Untreated 32Dcl3 cell lines expressing oncogenic tyrosine kinases or cells treated with small molecule inhibitors"'
GSE11794-GPL83_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"In our microarray study, we have total 22 samples from four different cell lines expressing BCR-ABL, TEL-ABL, FLT3-ITD or TEL-PDGF-betaR.  Each cell line was treated with specific small molecule inhibitors for 4 hours, then RNA was extracted and cRNA was hybridized to Affymetrix U74 oligonucleotide arrays. Untreated cells or cells treated with unrelated inhibitors were used as controls or references.  We have three replicates and six references obtained from three independent experiments for cells expressing BCR-ABL or FLT3-ITD.  We have one treated and one untreated sample for each cell line expressing TEL-ABL or TEL-PDGF-beta-R."'
GSE11794-GPL83_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"In our microarray study, we have total 22 samples from four different cell lines expressing BCR-ABL, TEL-ABL, FLT3-ITD or TEL-PDGF-betaR.  Each cell line was treated with specific small molecule inhibitors for 4 hours, then RNA was extracted and cRNA was hybridized to Affymetrix U74 oligonucleotide arrays. Untreated cells or cells treated with unrelated inhibitors were used as controls or references.  We have three replicates and six references obtained from three independent experiments for cells expressing BCR-ABL or FLT3-ITD.  We have one treated and one untreated sample for each cell line expressing TEL-ABL or TEL-PDGF-beta-R."'
GSE11796_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Starting with our early global expression analyses of TCDD-treated human hepatoma cells {Puga, 2000 4679 /id}, the AHR transcriptional induction profile has been extensively studied, whether activated by TCDD, B[a]P or in the absence of exogenous ligands (reviewed in {Frericks, 2007 5618 /id}).  In addition to using prior knowledge to integrate expression profiles into the AHR gene target network, we performed a new set of expression profile analyses of wild type Hepa-1c1c7 and c35 cell lines and compared the responses in naïve cells with responses in TCDD or B[a]P exposed cells for 8 hours.  Results of our expression array studies are in close agreement with current knowledge."'
GSE11803_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We measured global skeletal muscle expression in sedentary and exercised mice treated with vehicle or PPARdelta ligand GW1516.  PPARdelta is a transcriptional regulator of muscle oxidative metabolism and fatigue resistance."'
GSE11803_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Sedentary and exercise trained C57Bl/6J mice were treated with vehicle or GW1516 for 4 weeks, followed by collection of quadriceps for gene expression analysis."'
GSE11804_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Exercise activates serine/threonine kinase AMPK and transcriptional factor PPARdelta that re-model metabolism and endurance capacity of skeletal muscle.  Whether and how synthetic activation of these molecules regulated muscle gene signature is unknown."'
GSE11804_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We have conducted skeletal muscle microarrays from mice treated with AMPK agoinst (AICAR), PPARdelta agonist (GW1516) or the combination of the two drugs to investigate the individual and interactive effects of the two on muscle genes."'
GSE11804_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"C57Bl/6J mice were treated with Vehicle, AICAR, GW1516 and the combination of two drugs for 6 days, followed by collection of quadriceps for gene expression analysis."'
GSE11808_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"The human colon cancer TK-4 was implanted orthotopically into cecal walls of 6-week-old male BALB/c nu/nu mice (Clea Japan, Tokyo, Japan). The animals were treated with TSU68 (400 mg/kg/day, twice-daily, p.o.) or vehicle from 7 days after orthotopic implantation. After one week of drug administration, livers were removed and total RNA was extracted."'
GSE11808_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"We established four different groups of mice; non-tumor-bearing and treated with vehicle alone (NT-Co), non-tumor-bearing and treated with TSU68 (NT-TSU), tumor-bearing and treated with vehicle (T-Co), and tumor-bearing and treated with TSU68 (T-TSU). NT-Co, T-Co and T-TSU group were applied to microarray analysis."'
GSE11826_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Identifying alterations of gene expression induced by two teratogenic agents which induce a similar phenotype"'
GSE11826_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Samples used for hybridization consisted of non-pooled (NP) RNA extracts from 8 groups in each of two time periods after drug administration: oil vehicle treated control embryonic limb bud mesoderm and ectoderm, phosphate buffered saline vehicle control embryonic limb bud mesoderm and ectoderm, acetazolamide treated embryonic limb bud mesoderm and ectoderm, and cadmium sulfate treated embryonic limb bud mesoderm and ectoderm. Forty-eight hybridization experiments were on non-pooled (NP) individual RNA extracts."'
GSE11826_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Samples used for hybridization consisted of non-pooled (NP) RNA extracts from 8 groups in each of two time periods after drug administration: oil vehicle treated control embryonic limb bud mesoderm and ectoderm, phosphate buffered saline vehicle control embryonic limb bud mesoderm and ectoderm, acetazolamide treated embryonic limb bud mesoderm and ectoderm, and cadmium sulfate treated embryonic limb bud mesoderm and ectoderm. Forty-eight hybridization experiments were on non-pooled (NP) individual RNA extracts."'
GSE11836_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"In our investigations of the molecular pathways of prostate tumorigenesis in Nkx3.1; Pten mutant mice using gene expression profiling, we now find that the AP-1 transcription factors, c-Jun and c-Fos, are significantly up-regulated during cancer progression. Forced expression of c-Fos and c-Jun in prostate cancer cells results in increased tumorigenicity, activation of Erk MAP kinase, and enhanced survival in the absence of androgens, which are hallmarks of disease progression. In humans, Jun and Fos proteins are significantly up-regulated during prostate cancer progression and significantly correlated with activation of Erk MAP kinase. Most notably, expression of Jun is associated with disease recurrence independent of other currently used prognostic indicators."'
GSE11845_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"A small molecule that safely mimics the ability of dietary restriction (DR) to delay age-related diseases in laboratory animals is greatly sought after. We and others have shown that resveratrol mimics effects of DR in lower organisms. In mice, we find that resveratrol induces gene expression patterns in multiple tissues that parallel those induced by DR and every-other-day feeding. Moreover, resveratrol-fed elderly mice shows a marked reduction in signs of aging including reduced albuminuria, decreased inflammation and apoptosis in the vascular endothelium, increased aortic elasticity, greater motor coordination, reduced cataract formation, and preserved bone mineral density. However, mice fed a standard diet did not live longer when treated with resveratrol beginning at mid-life. Our findings indicate that resveratrol treatment has a range of beneficial effects in mice but does not increase the longevity of ad libitum-fed animals when started mid-life."'
GSE11845_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"A small molecule that safely mimics the ability of dietary restriction (DR) to delay age-related diseases in laboratory animals is greatly sought after. We and others have shown that resveratrol mimics effects of DR in lower organisms. In mice, we find that resveratrol induces gene expression patterns in multiple tissues that parallel those induced by DR and every-other-day feeding. Moreover, resveratrol-fed elderly mice shows a marked reduction in signs of aging including reduced albuminuria, decreased inflammation and apoptosis in the vascular endothelium, increased aortic elasticity, greater motor coordination, reduced cataract formation, and preserved bone mineral density. However, mice fed a standard diet did not live longer when treated with resveratrol beginning at mid-life. Our findings indicate that resveratrol treatment has a range of beneficial effects in mice but does not increase the longevity of ad libitum-fed animals when started mid-life."'
GSE11850_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Knowledge of the range of genes directly regulated by the Ah receptor would facilitate integration of the complex physiologic mechanisms that regulate the response to its toxic ligands at a systems biology level.  In this report, we have combined multiple technologies and knowledge-bases to conduct an integrative genome-wide analysis of Ah receptor gene targets, and interpret the results to elucidate the underlying physiological functions of the AHR in mammals.  Specifically, we used chromatin immunoprecipitation and hybridization to promoter tiling arrays to map constitutive, B[a]P- and TCDD-induced Ah receptor binding sites in a mouse hepatoma cell line, incorporating gene expression data and information from predicted cis-binding elements and overlapping molecular concept signatures."'
GSE11850_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"In the study presented here, mouse hepa-1c1c7 cells and c35 mutant hepa-1c1c7 derived cells with AHR unable to bind DNA, were used to predict AHR binding targets.  Two biological replicates were performed each condition (the naïve state, treated with B[a]P, and treated with TCDD).  Four replicate chips were performed for non-specific IgG."'
GSE11858_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mammary gland tissue samples were obtained in gonadectomized (GDX) animals treated with vehicle (control group), or injected with E2 (0.05 µg mg/mouse) at 1, 3, 6, 12, 18 and 24h prior to necropsy."'
GSE11859_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Acquisition of granule neuron precursor identity and Hedgehog-induced medulloblastoma in mice."'
GSE11859_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Origins of the brain tumor, medulloblastoma, from stem cells or restricted pro-genitor cells are unclear. To investigate this, we activated oncogenic Hedgehog signaling in multipotent and lineage-restricted CNS progenitors. We observed that normal unipo-tent cerebellar granule neuron precursors (CGNP) derive from hGFAP+ and Olig2+ rhombic lip progenitors. Hedgehog activation in a spectrum of early and late stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and that they retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors."'
GSE11859_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Origins of the brain tumor, medulloblastoma, from stem cells or restricted pro-genitor cells are unclear. To investigate this, we activated oncogenic Hedgehog signaling in multipotent and lineage-restricted CNS progenitors. We observed that normal unipo-tent cerebellar granule neuron precursors (CGNP) derive from hGFAP+ and Olig2+ rhombic lip progenitors. Hedgehog activation in a spectrum of early and late stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and that they retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors."'
GSE11862_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"In the treated animals, axons of the optic nerve were crushed with fine forceps for 10 sec, 1 mm posterior to the globe, under direct visualization, within an intact meningeal sheath. Controls were contralateral eyes from the same animals in each group that had not been injured. After 6 hr eyes were enucleated and processed for tissue sectionin"'
GSE11870_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Ligand-mediated activation of the nuclear hormone receptor PPAR gamma lowers blood pressure and improves glucose tolerance in humans.  Two naturally occurring mutations (P467L, V290M) in the ligand binding domain of PPAR gamma have been described in humans that lead to severe insulin resistance and hypertension.  Experimental evidence suggests that these mutant versions of PPAR gamma act in a dominant negative fashion.  To better understand the molecular mechanisms underlying PPAR gamma action in the vasculature, we determined the global gene expression profile in primary aortic endothelial cells in response to endothelial cell specific expression of a dominant negative isoform of PPAR gamma (V290M)."'
GSE11884_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Furin is a proprotein convertase induced in activated T cells, reported to processes the anti-inflammatory cytokine TGFb-1.  Herein, we show that conditional deletion of furin in T cells allowed for normal T cell development but impaired the function of regulatory T cells and effector cells, which produced less TGFb-1.  Furin-deficient Treg cells, were less protective in a T cell transfer colitis model and failed to induce Foxp3 in normal T cells. Furin-deficient effector cells were inherently overly active and were resistant to suppressive activity of wild-type Tregs. Thus, our results indicate that furin is indispensable in maintaining peripheral tolerance, which is due, at least in part, to its nonredundant, essential function in regulating TGFb-1 production.  Targeting furin has emerged as a strategy in malignant and infectious disease.  The current work suggests that inhibiting furin might activate immune responses, but may result in a breakdown in peripheral tolerance. "'
GSE11898_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"Expression data from primary mesangial cells stimulated with DNA and RNA ligands"'
GSE11898_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We used microarrays to detail the global programme of gene expression that induced by 3P-RNA and Non-CpG DNA."'
GSE11898_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"PMC were stimulated with 3P-RNA and Non-CpG DNA for 6 hours and then total RNA was isolated for hybridization to MOE430_2 arrays."'
GSE11910_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Using isolation stress model, we showed that goblet cell-dependent mucosal barrier functions in the mouse rectum was more vulnerable to stress than the colon. We also found that isolation stress specifically stimulated IL-18 production only in the rectum. Furthermore, the crucial role of IL-18 in the stress response of the mouse rectum was confirmed using IL-18 knockout mice. Microarray analysis was used to assess the stress response and to identify responsible genes for the vulnerability of the mouse rectum to isolation stress."'
GSE11911_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Methods: In an ovalbumin-induced murine model of asthma we applied microarray gene expression analysis of the lung at different time points in the asthmatic process. Advanced statistical methods were used to relate gene expression changes to cellular processes and to integrate our results into multiple levels of information available in public databases. "'
GSE11924_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"After activation, CD4+ helper T (Th) cells differentiate"'
GSE11924_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"(C-X-C motif) receptor 5-expressing T follicular"'
GSE11933_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Gene expression changes in femur bone induced by skeletal muscle unloading"'
GSE11933_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Gene expression changes in femur bone induced by acute skeletal muscle unloading, which leads to physiological changes including muscle atrophy, weakness and results in bone remodelling and subsequent loss of bone mass, was investigated by hind-limb suspension (HLS) treatment of Male ICR mice (28–32 g body wt; Harlan, Indianapolis, IN). AgilentTM Whole Mouse Genome Oligo Microarrays were utilised to examine the effects of HLS on mRNA expression profiles of the femur bone in the hindlimbs of freely ambulating control and 24h HLS treated mice. Five independent biological replicates of this experiment were carried out."'
GSE11933_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Gene expression changes in femur bone induced by acute skeletal muscle unloading, which leads to physiological changes including muscle atrophy, weakness and results in bone remodelling and subsequent loss of bone mass, was investigated by hind-limb suspension (HLS) treatment of Male ICR mice (28–32 g body wt; Harlan, Indianapolis, IN). AgilentTM Whole Mouse Genome Oligo Microarrays were utilised to examine the effects of HLS on mRNA expression profiles of the femur bone in the hindlimbs of freely ambulating control and 24h HLS treated mice. Five independent biological replicates of this experiment were carried out."'
GSE11939_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Repeated exposure to cocaine causes sensitized behavioral responses and increased dendritic spines on medium spiny neurons of the nucleus accumbens (NAc). We find that cocaine regulates myocyte enhancer factor 2 (MEF2) transcription factors to control these two processes in vivo. Cocaine suppresses striatal MEF2 activity in part through a novel mechanism involving cAMP, the regulator of calmodulin signaling (RCS), and calcineurin. We show that reducing MEF2 activity in the NAc in vivo is required for the cocaine-induced increases in dendritic spine density. Surprisingly, we find that increasing MEF2 activity in the NAc, which blocks the cocaine-induced increase in dendritic spine density, enhances sensitized behavioral responses to cocaine. Together, our findings implicate MEF2 as a key regulator of structural synapse plasticity and sensitized responses to cocaine, and suggest that reducing MEF2 activity (and increasing spine density) in NAc may be a compensatory mechanism to limit long-lasting maladaptive behavioral responses to cocaine."'
GSE11939_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Repeated exposure to cocaine causes sensitized behavioral responses and increased dendritic spines on medium spiny neurons of the nucleus accumbens (NAc). We find that cocaine regulates myocyte enhancer factor 2 (MEF2) transcription factors to control these two processes in vivo. Cocaine suppresses striatal MEF2 activity in part through a novel mechanism involving cAMP, the regulator of calmodulin signaling (RCS), and calcineurin. We show that reducing MEF2 activity in the NAc in vivo is required for the cocaine-induced increases in dendritic spine density. Surprisingly, we find that increasing MEF2 activity in the NAc, which blocks the cocaine-induced increase in dendritic spine density, enhances sensitized behavioral responses to cocaine. Together, our findings implicate MEF2 as a key regulator of structural synapse plasticity and sensitized responses to cocaine, and suggest that reducing MEF2 activity (and increasing spine density) in NAc may be a compensatory mechanism to limit long-lasting maladaptive behavioral responses to cocaine."'
GSE11939_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mice were treated for 7 days with daily injections of cocaine (20 mg/kg) and sacrificed 24 hrs later. Chromatin from bilateral punches of NAc was immunoprecipitated with an antibody against MEF2A as described previously with minor modifications (Renthal et al., 2007). Chromatin was sonicated to an average of ~500 bp and immunoprepitated with antibody against MEF2A (Santa Cruz, sc-313) or an IgG control (Upstate/Millipore).  Antibody-bound chromatin was precipitated using Protein A beads from Upstate (06-157), which were washed with low salt, high salt, and LiCl buffers to remove non-specific DNA binding. Eluted chromatin was reverse-crosslinked at 65oC in the presence of proteinase K and EDTA. DNA was purified by chloroform extraction/ethanol precipitation and the enrichment of specific promoters was amplified by ligation-mediated PCR for genome-wide analysis (Sikder et al., 2006).  Amplified DNA was then labeled with Cy3 (input-enriched) or Cy5 (MEF2-enriched) and hybridized to Nimblegen (Madison, WI) MM8 mouse promoter arrays. Bilateral nucleus accumbens from eight mice were pooled for microarray analysis."'
GSE11961_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"To obtain insight into the genetic basis of the increase of functional activity of memory B cells over time, we compared the gene expression profiles of day 7 and day 40 NP-specific/IgG1 memory B cells, GC B cells and plasma cells in immunized WT mice and naïve B cells, before and after activation in vitro."'
GSE11961_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"Total RNAs in three replicates of NP-specific/IgG1 memory B cells, GC B cells and plasma cells in immunized WT mice at day 7 and 40 postimmunization and naïve follicular and marginal zone B cells, before and after activation in vitro, were amplified and labeled according to the Affymetrix's instructions. cRNA was hybridized to Mouse Genome 430 2.0 GeneChips (Affymetrix)."'
GSE11963_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"RelA and RelB-dependent transcriptome analysis in lymphotoxin-ß receptor stimulated mouse embryonic fibroblasts"'
GSE11963_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Background: Lymphotoxin signaling via the lymphotoxin-β receptor (LTβR) has been implicated in several biological processes, ranging from development of secondary lymphoid organs, maintenance of splenic tissue, host defense against pathogens, autoimmunity, and lipid homeostasis. The major transcription factor that is activated by LTβR crosslinking is NF-κB. Two signaling pathways have been described that result in the activation of classical p50-RelA and alternative p52-RelB NF-κB heterodimers."'
GSE11963_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Results: Using microarray analysis, we investigated the transcriptional response downstream of the LTβR in mouse embryoni fibroblasts (MEF) and its regulation by the RelA and RelB subunits of NF-κB. We describe novel LTβR-responsive genes that are regulated by RelA and/or RelB. Interestingly, we found that the majority of LTβR-regulated genes require the presence of both RelA and RelB, suggesting significant crosstalk between the two NF-κB activation pathways. Gene Ontology (GO) analysis confirmed that LTβR-NF-κB target genes are predominantly involved in the regulation of immune responses. However, other biological processes, such as apoptosis/cell death, cell cycle, angiogenesis, and taxis were also regulated by LTβR signaling. Moreover, we show that activation of the LTβR inhibits the expression of a key adipogenic transcription factor, peroxisome proliferator activated receptor-γ (pparg), suggesting that LTβR signaling may interfere with adipogenic differentiation."'
GSE11963_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Conclusions: Thus, microarray analysis of LTβR-stimulated fibroblasts revealed further insight into the transcriptional response of LTβR signaling and its regulation by the NF-κB family members RelA and RelB."'
GSE11978_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Gene expression profiling of peripheral blood and alveolar recruited mononuclear phagocytes in Pam3CSK4 treated mice"'
GSE11981-GPL1261_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Gene expression profiling of HhAntag-treated pancreatic xenografts"'
GSE11981-GPL1261_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Four vehicle-treated and four HhAntag-treated pancreatic xenograft tumors were profiled for gene expression changes using Affymetrix U133 Plus 2.0 and Affymetrix Mouse Genome 430 2.0 arrays."'
GSE11981-GPL570_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Gene expression profiling of HhAntag-treated pancreatic xenografts"'
GSE11981-GPL570_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Four vehicle-treated and four HhAntag-treated pancreatic xenograft tumors were profiled for gene expression changes using Affymetrix U133 Plus 2.0 and Affymetrix Mouse Genome 430 2.0 arrays."'
GSE12008-GPL4134_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"LMX1B is a LIM-homeodomain transcription factor essential for development. Putative LMX1B target genes have been identified through mouse gene targeting studies; however, in the absence of in vivo molecular characterization of their regulation, their identity as direct LMX1B targets remains hypothetical. We describe here the first molecular characterization of LMX1B target gene regulation. A tetracycline-inducible expression system and microarray analysis showed that a subset of NF-kappa B target genes, including IL-6 and IL-8 are upregulated in LMX1B-expressing HeLa cells. Chromatin immunoprecipitation assays revealed that LMX1B binds to the proximal promoter region of IL-6 and IL-8 in vivo, in the vicinity of the characterized kappa B site, and that LMX1B recruitment correlates with an increased NF-kappa B DNA association. Inhibition of NF-kappa B activity by short interfering RNA-mediated knock-down of p65 impairs LMX1B-dependent induction of NF-kappa B target genes, while activation of NF-kappa B activity by TNF-alpha results in a synergistic induction of these genes by LMX1B. IL-6 promoter-driven reporter assays showed that the kappa B site and an adjacent putative LMX1B binding motif are both involved in LMX1B-mediated transcription. Expression of a number of NF-kappa B target genes is affected in the kidney of Lmx1b-/- knock-out mice, thus supporting the biological relevance of the data obtained in the human cell line. Together, these data demonstrate for the first time that LMX1B directly regulates transcription of a subset of NF-kappa B target genes in cooperation with nuclear p50/p65 NF-kappa B."'
GSE12008-GPL4134_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"LMX1B is a LIM-homeodomain transcription factor essential for development. Putative LMX1B target genes have been identified through mouse gene targeting studies; however, in the absence of in vivo molecular characterization of their regulation, their identity as direct LMX1B targets remains hypothetical. We describe here the first molecular characterization of LMX1B target gene regulation. A tetracycline-inducible expression system and microarray analysis showed that a subset of NF-kappa B target genes, including IL-6 and IL-8 are upregulated in LMX1B-expressing HeLa cells. Chromatin immunoprecipitation assays revealed that LMX1B binds to the proximal promoter region of IL-6 and IL-8 in vivo, in the vicinity of the characterized kappa B site, and that LMX1B recruitment correlates with an increased NF-kappa B DNA association. Inhibition of NF-kappa B activity by short interfering RNA-mediated knock-down of p65 impairs LMX1B-dependent induction of NF-kappa B target genes, while activation of NF-kappa B activity by TNF-alpha results in a synergistic induction of these genes by LMX1B. IL-6 promoter-driven reporter assays showed that the kappa B site and an adjacent putative LMX1B binding motif are both involved in LMX1B-mediated transcription. Expression of a number of NF-kappa B target genes is affected in the kidney of Lmx1b-/- knock-out mice, thus supporting the biological relevance of the data obtained in the human cell line. Together, these data demonstrate for the first time that LMX1B directly regulates transcription of a subset of NF-kappa B target genes in cooperation with nuclear p50/p65 NF-kappa B."'
GSE12008-GPL4134_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Human subset (GSM303547-GSM303550): Two biological replicates of non-expressing HtTA-LMX1B cells (grown in doxycycline-containing medium) and of LMX1B-expressing HtTA-LMX1B cells (grown for 4 days in doxycycline-free medium) were processed for gene expression array analyses using an Affymetrix platform."'
GSE12024-GPL75_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"NZB/WF1 female mice spontaneously develop autoimmune lupus nephritis. Expression profiling of kidney tissue from (a) 12 week NZB/W F1 female mice defined as asymptomatic for lupus nephritis, (b) 36 and 42 week NZB/W F1 female mice defined as diseased/symptomatic for lupus nephritis and (c) 36 and 42 week NZB/W F1 female mice that are diseased/symptomatic for lupus nephritis and treated with Sirolimus was carried out. The goal of the study was to identify genes associated with lupus nephritis and modulated by Sirolimus, an inhibitor of mTOR. In addition,  lupus nephritis genes resistant to Sirolimus therapy were also identfied"'
GSE12024-GPL76_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"NZB/WF1 female mice spontaneously develop autoimmune lupus nephritis. Expression profiling of kidney tissue from (a) 12 week NZB/W F1 female mice defined as asymptomatic for lupus nephritis, (b) 36 and 42 week NZB/W F1 female mice defined as diseased/symptomatic for lupus nephritis and (c) 36 and 42 week NZB/W F1 female mice that are diseased/symptomatic for lupus nephritis and treated with Sirolimus was carried out. The goal of the study was to identify genes associated with lupus nephritis and modulated by Sirolimus, an inhibitor of mTOR. In addition,  lupus nephritis genes resistant to Sirolimus therapy were also identfied"'
GSE12025_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Comparison of endocrine enriched genes in islet beta cells versus induced beta cells"'
GSE12025_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Endocrine enriched genes in adult islet beta cells were identified and compared with that of induced beta cells (with M3 transcription factors) in adult.  The control sample is non-beta pancreatic cells."'
GSE12025_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Gene expression profile comparison of 3 samples, 3 independent repeats for each sample indicate a high degree of similarity between endogenous and induced beta cells in adult mouse."'
GSE12028_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins."'
GSE12028_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins."'
GSE12036_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype. "'
GSE12067_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"The growth factor interleukin-3 (IL-3) promotes the survival and growth of multipotent hematopoietic progenitors and stimulates myelopoiesis.  It has also been reported to oppose terminal granulopoiesis and to support leukemic cell growth through autocrine or paracrine mechanisms.  We used kinetic microarray, Northern Blotting and bioinformatics analysis of IL-3 dependent myeloblasts to determine whether IL-3 acts in part by regulating the rate of turnover of mRNA transcripts in specific functional pathways.  Our results indicate that exposure of myeloblasts to IL-3 causes immediate early stabilization of hundreds of transcripts in pathways relevant to myeloblast function.  Examples include transcripts associated with proliferation and leukemic transformation (pik3cd, myb, pim-1), hematopoietic development (cited2), differentiation control (cdkn1a) and RNA processing (BRF1, BRF2).  A domain in the 3’-utr of IL-6 that mediates IL-3 responsiveness contains AU-rich elements that bind proteins known to modulate mRNA stability, however a known destabilizing protein (AUF1) is shown not to mediate degradation in the absence of IL-3.    These findings support a model of IL-3 action through mRNA stability control and suggest that aberrant stabilization of this network of transcripts could contribute to growth patterns observed in leukemia."'
GSE12073_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"Expression data from transgenic Aire expressing pancreatic islets"'
GSE12077_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Cancer cells differentiate along specific lineages that largely determine their clinical and biologic behavior. Distinct cancer phenotypes from different cells and organs likely result from unique gene expression repertoires established during lineage commitment in the embryo and maintained after malignant transformation. We used comprehensive gene expression analysis to examine this concept in the prostate, an organ with a readily manipulable developmental program and a high propensity for cancer. We focused on gene expression changes in the murine prostate rudiment (Urogenital Sinus, UGS) at three time points during the first 48 hours of exposure to androgen, which initiates proliferation and invasion of prostate epithelial buds into surrounding mesenchyme."'
GSE12111_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer. It is not clear, however, whether there are any innate surveillants that ensure keratinocytes undergoing terminal differentiation, preventing the disease. IKKα induces keratinocyte terminal differentiation and its reduction promotes skin tumor development. However, its nature function in skin cancer is unknown. Here we found that mice with IKKα deletion in keratinocytes or in hair follicle keratinocytes developed a thickened epidermis and spontaneous squamous cell-like carcinomas. Inactivation of epidermal growth factor receptor (EGFR) or reintroduction of IKKα inhibited excessive mitosis, induced terminal differentiation, and prevented skin cancer through an EGFR-driven autocrine loop in mice. Thus, IKKα serves as an innate surveillant. "'
GSE12117_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Role of inherent strain differences in prenatally induced differential metabolic syndrome phenotype and gene expression"'
GSE12117_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"There is much evidence suggesting that gene-environment interactions underlying the developmental origins of the metabolic syndrome. Previously, we have induced a metabolic syndrome phenotype in mice though prenatal undernutrition; however, the C57BL/6J strain exhibited significantly more metrics of the metabolic syndrome than the A/J strain."'
GSE12139_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Colonic tissues from an acute TNBS-induced colitis model in SJL mice."'
GSE12139_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Experimental colitis is often used as a model for the inflammatory bowel diseases, ulcerative colitis and Crohn’s disease. Results identify the inflammatory processes during acute colitis in affected tissues from TNBS-treated susceptible 5-7 week old SJL mice."'
GSE12139_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Two-condition experiment, Treated vs Non-treated. Biological replicates: 4 treated, 4 non-treated. One replicate per array."'
GSE12142_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Expression profile from doxorubicine treated B16 melanoma cells"'
GSE12142_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We used microarrays to decipher the specific gene regulation in doxorubicine treated B16 mouse melanoma cells."'
GSE12142_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"B16 cells were treated with 1 microgram/ml of doxorubicine and the RNAs were purified at 0, 2, and 4h after the treatment."'
GSE12147_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The nuclear receptor PPARalpha is recognized as the primary target of the fibrate class of hypolipidemic drugs and mediates lipid lowering in part by activating a transcriptional cascade that induces genes involved in the catabolism of lipids.  We report here the characterization of three novel PPARalpha agonists with therapeutic potential for treating dyslipidemia.  These structurally related compounds display potent and selective binding to human PPARalpha and support robust recruitment of coactivator peptides in vitro.  These compounds markedly potentiate chimeric transcription systems in cell-based assays and strikingly lower serum triglycerides in vivo.  The transcription networks induced by these selective PPARalpha agonists were assessed by transcriptional profiling of mouse liver after acute and chronic treatment.  The induction of several known PPARalpha target genes involved with fatty acid metabolism were observed, reflecting the expected pharmacology associated with PPARalpha activation.  We also noted the downregulation of a number of genes related to immune cell function, the acute phase response, and glucose metabolism; suggesting that these compounds may have anti-inflammatory action in the mammalian liver. Taken together, these studies articulate the therapeutic promise of a selective PPARalpha agonist."'
GSE12147_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The nuclear receptor PPARalpha is recognized as the primary target of the fibrate class of hypolipidemic drugs and mediates lipid lowering in part by activating a transcriptional cascade that induces genes involved in the catabolism of lipids.  We report here the characterization of three novel PPARalpha agonists with therapeutic potential for treating dyslipidemia.  These structurally related compounds display potent and selective binding to human PPARalpha and support robust recruitment of coactivator peptides in vitro.  These compounds markedly potentiate chimeric transcription systems in cell-based assays and strikingly lower serum triglycerides in vivo.  The transcription networks induced by these selective PPARalpha agonists were assessed by transcriptional profiling of mouse liver after acute and chronic treatment.  The induction of several known PPARalpha target genes involved with fatty acid metabolism were observed, reflecting the expected pharmacology associated with PPARalpha activation.  We also noted the downregulation of a number of genes related to immune cell function, the acute phase response, and glucose metabolism; suggesting that these compounds may have anti-inflammatory action in the mammalian liver. Taken together, these studies articulate the therapeutic promise of a selective PPARalpha agonist."'
GSE12147_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Male C57Bl/6 mice (n=4 for all except 5 day treatment of 146-02 was n=2) were treated with the piperidine agonists for 24hr or 5 days at 1mg/kg/day, or water (vehicle) as control."'
GSE12156_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Transcriptional profile of mouse primary spleen B cells overexpresing miR181b-GFP vectors compared to B cells overexpressing control-GFP vectors"'
GSE12158_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Transcriptional profile of mouse primary spleen B cells overexpresing miR181b-GFP vectors compared to B cells overexpressing control-GFP vectors"'
GSE12186-GPL4134_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"microRNA  expression profile of activated primary B cells and miR181b overexpressing primary B cells"'
GSE12186-GPL7042_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"microRNA  expression profile of activated primary B cells and miR181b overexpressing primary B cells"'
GSE12186-GPL7076_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"microRNA  expression profile of activated primary B cells and miR181b overexpressing primary B cells"'
GSE12209_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"The adipocyte-derived hormone leptin maintains energy balance by acting on hypothalamic leptin receptors (Leprs) that trigger the signal transducer and activator of transcription 3 (Stat3). Although disruption of Lepr-Stat3 signaling promotes obesity in mice, other features of Lepr function, such as fertility, seem normal, pointing to the involvement of additional regulators. Here we show that the cyclic AMP responsive element–binding protein-1 (Creb1)-regulated transcription coactivator-1 (Crtc1) is required for energy balance and reproduction—Crtc1-/- mice are hyperphagic, obese and infertile. Hypothalamic Crtc1 was phosphorylated and inactive in leptin-deficient ob/ob mice; leptin administration increased amounts of dephosphorylated nuclear Crtc1. Dephosphorylated Crtc1 stimulated expression of the Cartpt and Kiss1 genes, which encode hypothalamic neuropeptides that mediate leptin’s effects on satiety and fertility. Crtc1 overexpression in hypothalamic cells increased Cartpt and Kiss1 gene expression, whereas Crtc1 depletion decreased it. Indeed, leptin enhanced Crtc1 activity over the Cartpt and Kiss1 promoters in cells overexpressing Lepr and these effects were disrupted by expression of a dominant-negative Creb1 polypeptide. As leptin administration increased recruitment of hypothalamic Crtc1 to Cartpt and Kiss1 promoters, our results indicate that the Creb1-Crtc1 pathway mediates the central effects of hormones and nutrients on energy balance and fertility."'
GSE12209_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"The adipocyte-derived hormone leptin maintains energy balance by acting on hypothalamic leptin receptors (Leprs) that trigger the signal transducer and activator of transcription 3 (Stat3). Although disruption of Lepr-Stat3 signaling promotes obesity in mice, other features of Lepr function, such as fertility, seem normal, pointing to the involvement of additional regulators. Here we show that the cyclic AMP responsive element–binding protein-1 (Creb1)-regulated transcription coactivator-1 (Crtc1) is required for energy balance and reproduction—Crtc1-/- mice are hyperphagic, obese and infertile. Hypothalamic Crtc1 was phosphorylated and inactive in leptin-deficient ob/ob mice; leptin administration increased amounts of dephosphorylated nuclear Crtc1. Dephosphorylated Crtc1 stimulated expression of the Cartpt and Kiss1 genes, which encode hypothalamic neuropeptides that mediate leptin’s effects on satiety and fertility. Crtc1 overexpression in hypothalamic cells increased Cartpt and Kiss1 gene expression, whereas Crtc1 depletion decreased it. Indeed, leptin enhanced Crtc1 activity over the Cartpt and Kiss1 promoters in cells overexpressing Lepr and these effects were disrupted by expression of a dominant-negative Creb1 polypeptide. As leptin administration increased recruitment of hypothalamic Crtc1 to Cartpt and Kiss1 promoters, our results indicate that the Creb1-Crtc1 pathway mediates the central effects of hormones and nutrients on energy balance and fertility."'
GSE12209_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"The adipocyte-derived hormone leptin maintains energy balance by acting on hypothalamic leptin receptors (Leprs) that trigger the signal transducer and activator of transcription 3 (Stat3). Although disruption of Lepr-Stat3 signaling promotes obesity in mice, other features of Lepr function, such as fertility, seem normal, pointing to the involvement of additional regulators. Here we show that the cyclic AMP responsive element–binding protein-1 (Creb1)-regulated transcription coactivator-1 (Crtc1) is required for energy balance and reproduction—Crtc1-/- mice are hyperphagic, obese and infertile. Hypothalamic Crtc1 was phosphorylated and inactive in leptin-deficient ob/ob mice; leptin administration increased amounts of dephosphorylated nuclear Crtc1. Dephosphorylated Crtc1 stimulated expression of the Cartpt and Kiss1 genes, which encode hypothalamic neuropeptides that mediate leptin’s effects on satiety and fertility. Crtc1 overexpression in hypothalamic cells increased Cartpt and Kiss1 gene expression, whereas Crtc1 depletion decreased it. Indeed, leptin enhanced Crtc1 activity over the Cartpt and Kiss1 promoters in cells overexpressing Lepr and these effects were disrupted by expression of a dominant-negative Creb1 polypeptide. As leptin administration increased recruitment of hypothalamic Crtc1 to Cartpt and Kiss1 promoters, our results indicate that the Creb1-Crtc1 pathway mediates the central effects of hormones and nutrients on energy balance and fertility."'
GSE12218_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Robust type I interferon (IFN-alpha/beta) production in plasmacytoid dendritic cells (pDCs) is critical for anti-viral immunity. Here we demonstrated a role for the mammalian target of rapamycin (mTOR) pathway in regulating interferon production by pDCs. Inhibition of mTOR or the ‘downstream’ mediators of mTOR p70S6K1,2 kinases during pDC activation via Toll-like receptor 9 (TLR9) blocked the interaction of TLR9 with the adaptor MyD88 and the subsequent activation of interferon response factor 7 (IRF7), resulting in impaired IFN-alpha production. Microarray analysis confirmed that inhibition of mTOR by the immunosuppressive drug  rapamycin suppressed anti-viral and anti-inflammatory gene expression. Consistent with this, targeting rapamycin-encapsulated microparticles to antigen-presenting cells in vivo resulted in a diminution of IFN-alpha production in response to CpG DNA or the yellow fever vaccine virus strain 17D.  Thus, mTOR signaling plays a critical role in TLR-mediated IFN-alpha responses by pDCs."'
GSE12218_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"pDCs were isolated from mouse spleen or human PBMC. The effect of rapamycin on pDCs IFN-alpha production as induced by TLR ligands was studied. The mechanism of rapamycin effect was dissected in RAW cell line."'
GSE12247_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The mammary gland develops mainly postnatally, when during pregnancy the epithelium grows out into the mammary fat pad and forms a network of epithelial ducts. During pregnancy, these ducts branch and  bud to form alveoli. These alveoli produce the milk during lactation. After 7 days of lactation, involution was induced by force weaning the pups. The newly formed epithelium undergoes apoptosis and is removed from the tissue by neighbouring epithelial cells. Tissue remodelling leads to a morphology resembling a gland of a pre-pregnant mouse. Microarray analysis was used to measure mRNA expression of genes during puberty, pregnancy, lactation and involution in a Balb/c mouse strain."'
GSE12262_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Three prototypic situation were investigated using two replications for each experimental point: STAT3+/+ versus STAT3-/- MEFs , STAT3+/+ versus STAT3+/+ treated with OSM and STAT3-/- versus STAT3-/- treated with OSM."'
GSE12275_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"FAN (Factor associated with neutral sphingomyelinase activation) is an adaptor protein that constitutively binds to TNF-R1. Microarray analysis was performed in fibroblasts derived from wild-type or FAN knockout mouse embryos to evaluate the role of FAN in TNF-induced gene expression."'
GSE12275_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"FAN (Factor associated with neutral sphingomyelinase activation) is an adaptor protein that constitutively binds to TNF-R1. Microarray analysis was performed in fibroblasts derived from wild-type or FAN knockout mouse embryos to evaluate the role of FAN in TNF-induced gene expression."'
GSE12284_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Gene expression changes in LPS-induced neuroinflammation"'
GSE12284_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Neuroinflammation plays a role in the progression of several neurodegenerative disorders. We used a lipolysaccharide (LPS) model of neuroinflammation to characterize the gene expression changes underlying the inflammatory and behavioral effects of neuroinflammation. A single intracerebroventricular injection of LPS (5 ug) was administered into the lateral ventricle of mice and, 24 hours later, we examined gene expression in the cerebral cortex and hippocampus using microarray technology. Gene Ontology (GO) terms for inflammation and the ribosome were significantly enriched by LPS, whereas GO terms associated with learning and memory had decreased expression. We detected 224 changed transcripts in the cerebral cortex and 170 in the hippocampus. Expression of Egr1 (also known as Zif268) and Arc, two genes associated with learning and memory, was significantly lower in the cortex, but not hippocampus, of LPS-treated animals. Overall, altered expression of these genes may underlie some of the inflammatory and behavioral effects of neuroinflammation."'
GSE12285_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Interleukin-1-induced gene expression in mouse dermal fibroblasts"'
GSE12285_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Interleukin-1 (IL-1) is produced from immune-activated cells upon infection and tissue injury, and stimulates a variety of cells expressing its receptor. IL-1 receptor activation results in intracellular signaling cascades that culminate in the activation of transcription factors such as NF-kappaB, AP-1, and C/EBPbeta. To identify genes whose expression is induced in response to IL-1, we performed DNA microarray analysis of IL-1-treated murine dermal fibroblasts (DFs). The gene expression patterns in control, untreated DFs and in DFs treated with IL-1 were compared."'
GSE12285_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Interleukin-1 (IL-1) is produced from immune-activated cells upon infection and tissue injury, and stimulates a variety of cells expressing its receptor. IL-1 receptor activation results in intracellular signaling cascades that culminate in the activation of transcription factors such as NF-kappaB, AP-1, and C/EBPbeta. To identify genes whose expression is induced in response to IL-1, we performed DNA microarray analysis of IL-1-treated murine dermal fibroblasts (DFs). The gene expression patterns in control, untreated DFs and in DFs treated with IL-1 were compared."'
GSE12285_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Interleukin-1 (IL-1) is produced from immune-activated cells upon infection and tissue injury, and stimulates a variety of cells expressing its receptor. IL-1 receptor activation results in intracellular signaling cascades that culminate in the activation of transcription factors such as NF-kappaB, AP-1, and C/EBPbeta. To identify genes whose expression is induced in response to IL-1, we performed DNA microarray analysis of IL-1-treated murine dermal fibroblasts (DFs). The gene expression patterns in control, untreated DFs and in DFs treated with IL-1 were compared."'
GSE12285_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Interleukin-1 (IL-1) is produced from immune-activated cells upon infection and tissue injury, and stimulates a variety of cells expressing its receptor. IL-1 receptor activation results in intracellular signaling cascades that culminate in the activation of transcription factors such as NF-kappaB, AP-1, and C/EBPbeta. To identify genes whose expression is induced in response to IL-1, we performed DNA microarray analysis of IL-1-treated murine dermal fibroblasts (DFs). The gene expression patterns in control, untreated DFs and in DFs treated with IL-1 were compared."'
GSE12285_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Total RNAs from untreated DFs (0 h) vs. IL-1-treated DFs (1 h, 2 h, or 4 h after IL-1 treatment) were isolated and analyzed using an Agilent DNA microarray platform. Hybridization was performed in duplicate for dye swapping."'
GSE12294_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Basal (intermediate) progenitors are the major source of neurons in the mammalian cerebral cortex. The molecular machinery governing basal progenitor biogenesis is unknown. Here we show that the zinc finger transcription factor Insm1 (insulinoma-associated 1) is expressed  specifically in progenitors undergoing neurogenic divisions and has a key role in basal progenitor formation. Mouse embryos lacking Insm1 contained half the number of basal progenitors and showed a marked reduction in cortical plate radial thickness. Forced premature expression of Insm1 in neuroepithelial cells resulted in their mitosis occurring at the basal (rather than apical) side of the ventricular zone and induced expression of the basal progenitor marker Tbr2. Remarkably,  these cells remained negative for Tis21, a marker of neurogenic progenitors, and did not generate neurons but underwent self-amplification. Our data imply that Insm1 is involved in the generation  and expansion of basal progenitors, a hallmark of cerebral cortex evolution."'
GSE12312_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Changes in gravitational force such as that experienced by astronauts during space flight induce a redistribution of fluids from the caudad to the cephalad portion of the body together with an elimination of normal head-to-foot hydrostatic pressure gradients. To assess brain gene profile changes associated with microgravity and fluid shift, a large-scale analysis of mRNA expression levels was performed in the brains of 2 weeks control and hindlimb-unloaded (HU) mice using cDNA microarrays. Although to different extent, all functional categories displayed significantly regulated genes indicating that considerable transcriptomic alterations are induced by HU. Interestingly, the TIC class (transport of small molecules and ions into the cells) had the highest percentage of up-regulated genes, while the most down-regulated genes were those of the JAE class (Cell junction, Adhesion, Extracellular Matrix). TIC genes comprised 16% of those whose expression was altered, including sodium channel, nonvoltage-gated 1 beta (Scnn1b), glutamate receptor (Grin1), voltage-dependent anion channel 1 (Vdac1), calcium channel beta 3 subunit (Cacnb3) and others. The analysis performed by GeneMAPP revealed several altered protein classes and functional pathways such as blood coagulation and immune response, learning and memory, ion channels and cell junction. In particular, data indicate that HU causes an alteration in hemostasis which resolves in a shift toward a more hyper-coagulative state with an increased risk of venous thrombosis. Furthermore, HU treatment seems to impact on key steps of synaptic plasticity and learning processes."'
GSE12313_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mll-AF4stop knock-in mice were treated with 5-FU and 5 days later their bone marrow infected ex vivo with either Cre-GFP to activate the Mll-AF4 fusion construct or with a control MIG-Cre retrovirus. GFP+ cells were sorted 2 days post-infection and cultured for 14 days under lymphoid growth conditions before total RNA was isolated for hybridization to Affymetrix expression microarrays."'
GSE12321_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Examining the transcriptional change in whole mouse (VM) brain miRNA expression during prion (22A) induced neurodegeneration in order to identify miRNAs that are differentially expressed. MicroRNAs (miRNAs) are small, non-coding RNA molecules which are emerging as key regulators of numerous cellular processes.  Compelling evidence links miRNAs to the control of neuronal development and differentiation, however, little is known about their role in neurodegeneration. De-regulation of a unique subset of miRNAs may suggest a conserved, disease-specific pattern of differentially expressed miRNAs is associated with prion–induced neurodegeneration.  "'
GSE12321_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"MiRNA extracted from the whole brains of 3 VM mice treated with mouse-adapted 22A scrapie strain were analyzed on GPL7118 (array was divided into top and bottom) for differential expression. Age-matched, PBS treated control mice were used for comparison (competitive hybridization). A technical replicate for each mouse was performed as well as a technical replicate for each of the dye-swaps. "'
GSE12322_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Examining the transcriptional change in whole mouse (VM) brain miRNA expression during prion (22A) induced neurodegeneration in order to identify miRNAs that are differentially expressed. MicroRNAs (miRNAs) are small, non-coding RNA molecules which are emerging as key regulators of numerous cellular processes.  Compelling evidence links miRNAs to the control of neuronal development and differentiation, however, little is known about their role in neurodegeneration. De-regulation of a unique subset of miRNAs may suggest a conserved, disease-specific pattern of differentially expressed miRNAs is associated with prion–induced neurodegeneration."'
GSE12322_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"MiRNA extracted from the whole brains of 4 VM mice treated with mouse-adapted 22A scrapie strain were analyzed on GPL7121 (array was divided into top and bottom) for differential expression. Age-matched, PBS treated control mice were used for comparison (competitive hybridization). A technical replicate for each mouse was performed as well as a technical replicate for each of the dye-swaps."'
GSE12337_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The primary aim of this study was to identify the processes and signaling pathways regulated by PPARalpha in hearts challenged by a chronic pressure overload by means of whole genome transcriptomic analysis. Second, we wanted to gain insight how PPARalpha modulates the identified processes, e.g. by trans-activation or by trans-repression."'
GSE12346_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Th2 cells enable humoral immunity and host-defense to parasites. Whereas IL-4 drives Th2 differentiation and IL-2 is important later in this process by augmenting IL4 chromatin accessibility, we demonstrate that IL-2 serves an essential early role in regulating IL-4Rα expression by inducing binding of Stat5a and Stat5b to the IL4ra locus, with sustained binding during Th2 differentiation.  Although IL-4 induces IL-4Rα expression, TCR-induced IL-4Rα expression was unexpectedly normal in ILr-/- but profoundly diminished in IL2-/- T cells. Remarkably, enforced IL-4Rα expression rescued Th2 differentiation in IL2-/- cells. These results reveal a novel function for IL-2, with IL-2 via Stat5 providing an early signal for IL4ra induction, thereby priming cells for Th2 differentiation and promoting/maintaining IL-4Rα expression in Th2-committed cells."'
GSE12356_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The chromatin regulator Aiolos and the transcriptional coactivator OBF-1 have been implicated in regulating aspects of B cell maturation and activation. Mice lacking either of these factors have a largely normal early B cell development. However, when both factors are eliminated simultaneously a block is uncovered at the transition between pre-B and immature B cells, indicating that these proteins exert a critical function in developing B lymphocytes. In mice deficient for Aiolos and OBF-1, the numbers of immature B cells are reduced, small pre-BII cells are increased and a significant impairment in immunoglobulin light chain DNA rearrangement is observed. We identified genes whose expression is deregulated in the pre-B cell compartment of these mice. In particular, we found that components of the pre-BCR, such as the surrogate light chain genes l5l5 and VpreB, fail to be efficiently silenced in double-mutant mice. Strikingly, developmentally regulated nuclear repositioning of the l5l5 gene is impaired in pre-B cells lacking OBF-1 and Aiolos. These studies uncover a novel role for OBF-1 and Aiolos in controlling the transcription and nuclear organization of genes involved in pre-BCR function."'
GSE12361_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"DNA was immunoprecipitated with anti-dimethyl-H3K79 antibodies from purified marrow preB cells of normal mice or animals made leukemic by activation of an MLL-AF4 fusion. The ChIP DNA was then hybridized to Affymetrix promoter tiling microarrays."'
GSE12362_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"DNA was immunoprecipitated with anti-dimethyl-H3K79 antibodies from bone marrow of mice made leukemic by activation of an MLL-AF4 fusion. The ChIP DNA was then hybridized to Affymetrix promoter tiling microarrays."'
GSE12367_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"To compare the gene expression profiles of Deaf-1-transduced MECs relative to Deaf-1-deficient MECs, Affymetrix analysis was performed using the GeneChip® Mouse Expression Set 430 2.0 array which comprises 39,000 transcripts on a single array.  Total RNA was harvested from two independent clones (C1 and E1) infected with either control or Deaf-1-expressing retrovirus making 4 samples in total.  Clones C1 and E1 were treated as biological replicates in the subsequent analysis."'
GSE12367_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"To compare the gene expression profiles of Deaf-1-transduced MECs relative to Deaf-1-deficient MECs, Affymetrix analysis was performed using the GeneChip® Mouse Expression Set 430 2.0 array which comprises 39,000 transcripts on a single array.  Total RNA was harvested from two independent clones (C1 and E1) infected with either control or Deaf-1-expressing retrovirus making 4 samples in total.  Clones C1 and E1 were treated as biological replicates in the subsequent analysis."'
GSE12387_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"This study examined NAc gene expression in a pair short-term selected lines bred for high or low response to methamphetamine (MA).  We sought to identify candidate genes preferentially expressed among individuals showing either large or small acute responses to MA.  Additionally, we sought to identify genes and networks differentially expressed by MA exposure within these divergent lines."'
GSE12388_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"The prevention of autoimmunity requires elimination of self-reactive T cells during their development and maturation. Expression of diverse self-antigens by stromal cells in the thymus is essential to this process, and depends, in part, on the activity of the Autoimmune Regulator (Aire) gene. Here we report the identification of extrathymic Aire-expressing cells (eTACs) resident within the secondary lymphoid organs. These stromally-derived eTACs express a diverse array of unique self-antigens and are capable of interacting with and deleting naive autoreactive T cells. Using two-photon microscopy we observe stable, antigen-specific interactions between eTACs and autoreactive T cells. We propose that such a secondary network of self-antigen-expressing stromal cells may help reinforce immune tolerance by preventing the maturation of autoreactive T cells that escape thymic negative selection."'
GSE12389_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We demonstrate diverse roles of interferon–gamma (IFN-γ) in the induction and regulation of immune-mediated inflammation using a transfer model of autoimmune diabetes. The diabetogenic CD4+BDC2.5 (BDC) T cell clone upon transfer into NOD.scid mice induced destruction of islets of Langerhans leading to diabetes. Administration of a neutralizing antibody to IFN-γ (H22) resulted in long term protection (LTP) from diabetes, with inflammation but persistence of a significant, albeit decreased numbers of β-cells. BDC T cells were a mixture of cells expressing high, intermediate and low levels of the T cell receptor. Clonotype-low BDC T cells were required for LTP. Furthermore, islet infiltrating leukocytes in the LTP mice contained Foxp3+CD4 T cells. Islet inflammation in both diabetic and LTP mice was characterized by heavy infiltration of macrophages. Gene expression profiles indicated that macrophages in diabetic mice were M1-type, while LTP mice contained M2-differentiated. The LTP was abolished if mice were treated with either an antibody depleting CD4 T cells, or a neutralizing antibody to CTLA-4, in this case, only at a late stage. Neutralization of IL-10, TGF-β, GITR or CD25 had no effect. Transfer of only clonotype-high expressing BDC T cells induced diabetes but in contrast, H22 antibodies did not inhibit diabetes. While clonotype high T cells induced diabetes even when IFN-γ was neutralized, paradoxically, there was reduced inflammation and no diabetes if host myeloid cells lacked IFN-γ receptor. Hence, using monoclonal CD4 T cells, IFN-γ can have a wide diversity of roles, depending on the setting of the immune process."'
GSE12389_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We demonstrate diverse roles of interferon–gamma (IFN-γ) in the induction and regulation of immune-mediated inflammation using a transfer model of autoimmune diabetes. The diabetogenic CD4+BDC2.5 (BDC) T cell clone upon transfer into NOD.scid mice induced destruction of islets of Langerhans leading to diabetes. Administration of a neutralizing antibody to IFN-γ (H22) resulted in long term protection (LTP) from diabetes, with inflammation but persistence of a significant, albeit decreased numbers of β-cells. BDC T cells were a mixture of cells expressing high, intermediate and low levels of the T cell receptor. Clonotype-low BDC T cells were required for LTP. Furthermore, islet infiltrating leukocytes in the LTP mice contained Foxp3+CD4 T cells. Islet inflammation in both diabetic and LTP mice was characterized by heavy infiltration of macrophages. Gene expression profiles indicated that macrophages in diabetic mice were M1-type, while LTP mice contained M2-differentiated. The LTP was abolished if mice were treated with either an antibody depleting CD4 T cells, or a neutralizing antibody to CTLA-4, in this case, only at a late stage. Neutralization of IL-10, TGF-β, GITR or CD25 had no effect. Transfer of only clonotype-high expressing BDC T cells induced diabetes but in contrast, H22 antibodies did not inhibit diabetes. While clonotype high T cells induced diabetes even when IFN-γ was neutralized, paradoxically, there was reduced inflammation and no diabetes if host myeloid cells lacked IFN-γ receptor. Hence, using monoclonal CD4 T cells, IFN-γ can have a wide diversity of roles, depending on the setting of the immune process."'
GSE12389_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"We demonstrate diverse roles of interferon–gamma (IFN-γ) in the induction and regulation of immune-mediated inflammation using a transfer model of autoimmune diabetes. The diabetogenic CD4+BDC2.5 (BDC) T cell clone upon transfer into NOD.scid mice induced destruction of islets of Langerhans leading to diabetes. Administration of a neutralizing antibody to IFN-γ (H22) resulted in long term protection (LTP) from diabetes, with inflammation but persistence of a significant, albeit decreased numbers of β-cells. BDC T cells were a mixture of cells expressing high, intermediate and low levels of the T cell receptor. Clonotype-low BDC T cells were required for LTP. Furthermore, islet infiltrating leukocytes in the LTP mice contained Foxp3+CD4 T cells. Islet inflammation in both diabetic and LTP mice was characterized by heavy infiltration of macrophages. Gene expression profiles indicated that macrophages in diabetic mice were M1-type, while LTP mice contained M2-differentiated. The LTP was abolished if mice were treated with either an antibody depleting CD4 T cells, or a neutralizing antibody to CTLA-4, in this case, only at a late stage. Neutralization of IL-10, TGF-β, GITR or CD25 had no effect. Transfer of only clonotype-high expressing BDC T cells induced diabetes but in contrast, H22 antibodies did not inhibit diabetes. While clonotype high T cells induced diabetes even when IFN-γ was neutralized, paradoxically, there was reduced inflammation and no diabetes if host myeloid cells lacked IFN-γ receptor. Hence, using monoclonal CD4 T cells, IFN-γ can have a wide diversity of roles, depending on the setting of the immune process."'
GSE12394_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"miRNA expression profiling of murine MYC-dependent lymphoma cell lines harboring the MYC-transgene in a Tet-off system comparing control untreated lymphoma cells (high MYC expression state) with 18hours Dox treated lymphoma cells (low MYC expression state)."'
GSE12419-GPL2884_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The human CDKN2A locus encodes two distinct proteins, p16(INK4A) and p14(ARF) [mouse p19(Arf)], designated INK4A and ARF herein, that are translated from alternatively spliced mRNAs.  Human ARF is implicated as a tumor suppressor gene, mainly in association with the simultaneous deletion of INK4A.  However, questions remain as to whether loss of ARF alone is sufficient to drive tumorigenesis.  Here we report that mice deficient for Arf are susceptible to accelerated asbestos-induced malignant mesothelioma (MM).  MMs arising in Arf (+/-) mice consistently exhibit biallelic inactivation of Arf, but unexpectedly, do not acquire additional recurrent genetic alterations that we previously identified in asbestos-induced MMs arising in Nf2 (+/-) mice.  Array CGH analysis was used to detect a recurrent deletion at chromosome 4C6.  A candidate in this region, Faf1 (FAS-associated factor 1), was further explored because it encodes a protein implicated in tumor cell survival and in the pathogenesis of some human tumor types.  We confirmed hemizygous loss of Faf1 and down regulation of Faf1 protein in a series of MMs from Arf (+/-) mice, and then showed that Faf1 regulates TNFalpha-mediated NFkappaB signaling, a mechanism previously implicated in asbestos-induced oncogenesis of human mesothelial cells.  Collectively, these investigations divulge important information regarding the significance of Arf inactivation in MM pathogenesis, and implicate Faf1 as a key component in the TNFalpha/NFkappaB signaling node that has now been independently implicated in the asbestos-induced oncogenesis."'
GSE12419-GPL4092_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The human CDKN2A locus encodes two distinct proteins, p16(INK4A) and p14(ARF) [mouse p19(Arf)], designated INK4A and ARF herein, that are translated from alternatively spliced mRNAs.  Human ARF is implicated as a tumor suppressor gene, mainly in association with the simultaneous deletion of INK4A.  However, questions remain as to whether loss of ARF alone is sufficient to drive tumorigenesis.  Here we report that mice deficient for Arf are susceptible to accelerated asbestos-induced malignant mesothelioma (MM).  MMs arising in Arf (+/-) mice consistently exhibit biallelic inactivation of Arf, but unexpectedly, do not acquire additional recurrent genetic alterations that we previously identified in asbestos-induced MMs arising in Nf2 (+/-) mice.  Array CGH analysis was used to detect a recurrent deletion at chromosome 4C6.  A candidate in this region, Faf1 (FAS-associated factor 1), was further explored because it encodes a protein implicated in tumor cell survival and in the pathogenesis of some human tumor types.  We confirmed hemizygous loss of Faf1 and down regulation of Faf1 protein in a series of MMs from Arf (+/-) mice, and then showed that Faf1 regulates TNFalpha-mediated NFkappaB signaling, a mechanism previously implicated in asbestos-induced oncogenesis of human mesothelial cells.  Collectively, these investigations divulge important information regarding the significance of Arf inactivation in MM pathogenesis, and implicate Faf1 as a key component in the TNFalpha/NFkappaB signaling node that has now been independently implicated in the asbestos-induced oncogenesis."'
GSE12421_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_title	"Analysis of OBF-1 overexpression in early B cells"'
GSE12421_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"OBF1, also known as Bob.1 or OCA-B, is a B lymphocyte-specific transcription factor which coactivates Oct1 and Oct2 on B cell specific promoters. So far, the function of OBF1 has been mainly identified in late stage B cell populations. The central defect of OBF1 deficient mice is a severely reduced immune response to T cell-dependent antigens and a lack of germinal center formation in the spleen. Relatively little is known about a potential function of OBF1 in developing B cells. Here we have generated transgenic mice overexpressing OBF1 in B cells under the control of the immunoglobulin heavy chain promoter and enhancer. Surprisingly, these mice have greatly reduced numbers of follicular B cells in the periphery and have a compromised immune response. Furthermore, B cell differentiation is impaired at an early stage in the bone marrow. A first block is observed during B cell commitment and a second differentiation block is seen at the large preB2 cell stage. The cells that succeed to escape the block and to differentiate into mature B cells have post-translationally downregulated the expression of transgene, indicating that expression of OBF1 beyond the normal level early in B cell development is deleterious. Indeed ID3, which is a negative regulator of B cell differentiation, is upregulated in the EPLM and preB cells of the transgenic mice. Furthermore ID3 promoter contains an octamer site suggesting that it is a potential OBF-1 direct target gene. These results provide evidence that OBF1 expression has to be tightly regulated in early B cells to allow efficient B lymphocyte differentiation."'
GSE12425_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_title	"Dox-regulated Notch4 overexpression in mouse ES cells redirects hemagioblasts to a cardiac fate."'
GSE12425_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Bry-GFP+/Flk-1+ cells, sorted from EB's derived from ES cell differentiation cultures exposed to serum for 3.5 days, were allowed to reaggregate for 24 in the presence or absence of doxycycline, and the total RNA harvested at 4, 12, 24, 48, and 96 hours post Dox induction for microarray analysis.  The induced populations were compared to non-induced population harvested at the same time points."'
GSE12426_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Control-ACSF: cultured hippocampal slices were incubated with ACSF for 2 hours and were analysed on whole-genome expression chips to determine the gene expression profile. This group was used as controls for IS-treated groups and ACSF+DIDS-treated grous."'
GSE12426_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"IS: cultured hippocampal slices were treated wtih IS for 2 hours and the gene expression was analyzed and compared with the control group."'
GSE12426_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"IS+DIDS: cultured slices were treated with both IS and DIDS for 2 hours and the gene expression profile was determined. Differentially expression genes were identified by comparing with IS group."'
GSE12441_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"A fundamental question in biology is how an undifferentiated field of cells acquires spatial pattern and undergoes coordinated differentiation. The development of the vertebrate limb is an important paradigm for understanding these processes. The skeletal and connective tissues of the developing limb all derive from a population of multipotent progenitor cells located in its distal tip. During limb outgrowth, these progenitors segregate into a chondrogenic lineage, located in the center of the limb bud, and soft connective tissue lineages located in its periphery. We report that the interplay of two families of signaling proteins, fibroblast growth factors (FGFs) and Wnts, coordinate the growth of the multipotent progenitor cells with their simultaneous segregation into these lineages. FGF and Wnt signals act together to synergistically promote proliferation while maintaining the cells in an undifferentiated, multipotent state, but act separately to determine cell lineage specification. Withdrawal of both signals results in cell cycle withdrawal and chondrogenic differentiation. Continued exposure to Wnt however, maintains proliferation and re-specifies the cells towards the soft connective tissue lineages. We have identified target genes that are synergistically regulated by Wnts and Fgfs, and show how these factors actively suppress differentiation and promote growth. Finally, we show how the spatial restriction of Wnt and FGF signals to the limb ectoderm and to a specialized region of it, the apical ectodermal ridge, controls the distribution of cell behaviors within the growing limb, and guides the proper spatial organization of the differentiating tissues."'
GSE12441_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Cells derived from mouse embryonic stage 11.5 limb buds were cultured and treated with purified Wnt3a protein or vehicle controls. The transcriptional response was detected using spotted cDNA microarrays after 2 hrs or 4 hrs of treatment. 4 biological replicates were used per condition."'
GSE12464_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The Tec-family kinase Itk plays an important role during T-cell activation and function, and controls also conventional versus innate-like T-cell development. We have characterized the transcriptome of Itk-deficient CD3+ T-cells, including CD4+ and CD8+ subsets, using Affymetrix microarrays. The largest difference between Itk-/- and Wt CD3+ T-cells was found in unstimulated cells, e.g. for killer cell lectin-like receptors. Compared to anti-CD3-stimulation, anti-CD3/CD28 significantly decreased the number of transcripts suggesting that the CD28 co-stimulatory pathway is mainly independent of Itk. The signatures of CD4+ and CD8+ T-cell subsets identified a greater differential expression than in total CD3+ cells. Cyclosporin (CsA)-treatment had a stronger effect on transcriptional regulation than Itk-deficiency, suggesting that only a fraction of TCR-mediated calcineurin/NFAT-activation is dependent on Itk. Bioinformatic analysis of NFAT-sites of the group of transcripts similarly regulated by Itk-deficiency and CsA-treatment, followed by chromatin-immunoprecipitation, revealed NFATc1-binding to the Bub1, IL7R, Ctla2a, Ctla2b, and Schlafen1 genes. Finally, to identify transcripts that are regulated by Tec-family kinases in general, we compared the expression profile of Itk-deficient T-cells with that of Btk-deficient B-cells and a common set of transcripts was found. Taken together, our study provides a general overview about the global transcriptional changes in the absence of Itk."'
GSE12464_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"CD3+ T-cells from pooled suspensions of spleen and lymph nodes of Wt and Itk knockout mice on C57BL/6 background were isolated after negative depletion. Unstimulated as well as stimulated T-cells were studied. Stimulations were done with anti-CD3 (1 mg/ml) with or without anti-CD28 (3 mg/ml) in the presence or absence of CsA (1 mg/ml) for 24 hrs. For each stimulus, at least duplicate samples were used."'
GSE12465_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The Tec-family kinase Itk plays an important role during T-cell activation and function, and controls also conventional versus innate-like T-cell development. We have characterized the transcriptome of Itk-deficient CD3+ T-cells, including CD4+ and CD8+ subsets, using Affymetrix microarrays. The largest difference between Itk-/- and Wt CD3+ T-cells was found in unstimulated cells, e.g. for killer cell lectin-like receptors. Compared to anti-CD3-stimulation, anti-CD3/CD28 significantly decreased the number of transcripts suggesting that the CD28 co-stimulatory pathway is mainly independent of Itk. The signatures of CD4+ and CD8+ T-cell subsets identified a greater differential expression than in total CD3+ cells. Cyclosporin (CsA)-treatment had a stronger effect on transcriptional regulation than Itk-deficiency, suggesting that only a fraction of TCR-mediated calcineurin/NFAT-activation is dependent on Itk. Bioinformatic analysis of NFAT-sites of the group of transcripts similarly regulated by Itk-deficiency and CsA-treatment, followed by chromatin-immunoprecipitation, revealed NFATc1-binding to the Bub1, IL7R, Ctla2a, Ctla2b, and Schlafen1 genes. Finally, to identify transcripts that are regulated by Tec-family kinases in general, we compared the expression profile of Itk-deficient T-cells with that of Btk-deficient B-cells and a common set of transcripts was found. Taken together, our study provides a general overview about the global transcriptional changes in the absence of Itk."'
GSE12465_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"CD3+ CD4+ and CD8+ T-cells from pooled suspensions of spleen and lymph nodes of Wt and Itk knockout mice on C57BL/6 background were isolated after negative depletion. Unstimulated as well as stimulated T-cells were studied. Stimulations were done with anti-CD3 (1 mg/ml) for 24 hrs. For the CD4+ T-cells we collected triplicates from the Itk knockout mice and duplicates from the Wt group. For the CD8+ T-cells, we got duplicates from Itk knockout , while we obtained a single sample from Wt owing to the low cell yield for resting Wt CD8+ T-cells. After CD3-stimulation we got a single sample from the CD8+ subset of both Wt and Itk knockout, while for the CD4+ subsets we collected duplicates."'
GSE12489_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Animals were injected i.p. 100mg/kg phenobarbital or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the phenobarbital treated ones and hybridized to Sterolgene V1 arrays."'
GSE12498_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"Regulation of organ size is important for development and tissue homeostasis. In  Drosophila, Hippo signaling controls organ size by regulating the activity of a TEAD  transcription factor, Scalloped, through modulation of its coactivator protein Yki. The  role of mammalian Tead proteins in growth regulation, however, remains unknown.  Here we examined the role of mouse Tead proteins in growth regulation. In NIH3T3  cells, cell density and Hippo signaling regulated the activity of Tead proteins by  modulating nuclear localization of a Yki homologue, Yap, and the resulting change in  Tead activity altered cell proliferation. Tead2-VP16 mimicked Yap overexpression,  including increased cell proliferation, reduced cell death, promotion of EMT, lack of cell  contact inhibition, and promotion of tumor formation. Growth promoting activities of  various Yap mutants correlated with their Tead-coactivator activities. Tead2-VP16 and  Yap regulated largely overlapping sets of genes. However, only a few of the Tead/Yapregulated  genes in NIH3T3 cells were affected in Tead1-/-;Tead2-/- or Yap-/- embryos. Most  of the previously identified Yap-regulated genes were not affected in NIH3T3 cells or  mutant mice. In embryos, levels of nuclear Yap and Tead1 varied depending on cell  types. Strong nuclear accumulation of Yap and Tead1 were seen in myocardium,  correlating with requirements of Tead1 for proliferation. However, their distribution did  not always correlate with proliferation. Taken together, mammalian Tead proteins  regulate cell proliferation and contact inhibition as a transcriptional mediator of Hippo  signaling, but the mechanisms by which Tead/Yap regulate cell proliferation differ  depending on cell types, and Tead, Yap and Hippo signaling may play multiple roles in  mouse embryos."'
GSE12498_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Tead2-VP16-, Tead2-EnR-, Yap- and control vector-expressing cells were cultured at low or high density for RNA extraction and hybridization on Affymetrix microarrays."'
GSE12499_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The four transcription factors Oct4, Sox2, Klf4, and c-Myc can induce pluripotency in mouse and human fibroblasts. We previously described direct reprogramming of adult mouse neural stem cells (NSCs) by Oct4 and either Klf4 or c-Myc. NSCs endogenously express Sox2, c-Myc, and Klf4 as well as several intermediate reprogramming markers. Here we report that exogenous expression of the germline-specific transcription factor Oct4 is sufficient to generate pluripotent stem cells from adult mouse NSCs. These one-factor induced pluripotent stem (1F iPS) cells are similar to embryonic stem cells in vitro and in vivo. Not only can these cells be efficiently differentiated into NSCs, cardiomyocytes and germ cells in vitro, but they are also capable of teratoma formation and germline transmission in vivo. Our results demonstrate that Oct4 is required and sufficient to directly reprogram NSCs to pluripotency."'
GSE12503_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Despite a complete absence of intestinal mucin, mice lacking AGR2 appeared healthy but were highly susceptible to dextran sodium sulfate-induced experimental colitis, indicating a critical role for AGR2 in protection from environmental insults."'
GSE12506_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The concept of immune regulation/suppression has been well-established. With thymus-derived CD4 CD25  regulatory T (TR) cells, it became clear that a variety of additional peripherally induced TR cells play vital roles in protection from many harmful immune responses including intestinal inflammation. In the present study, we have analyzed in vivo-induced Ag-specific CD4 TR cells with respect to their molecular and functional phenotype. By comparative genomics we could show that these Ag-specific TR cells induced by chronic Ag stimulation in vivo clearly differ in their genetic program from naturally occurring thymus-derived CD4 CD25  TR cells. This distinct population of induced TR cells express neither CD25 nor the TR-associated transcription factor Foxp3. Strikingly, CD25 is not even up-regulated upon stimulation. Despite the lack in Foxp3 expression, these in vivo-induced CD25  TR cells are able to interfere with an Ag-specific CD8  T cell-mediated intestinal inflammation without significant increase in CD25 and Foxp3 expression. Thus, our results demonstrate that in vivo-induced Ag-specific TR cells represent a distinct population of Foxp3 CD25  TR cells with regulatory capacity both in vitro and in vivo."'
GSE12506_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"To define the molecular signature of Ag-specific in vivo-induced dtg CD25 TR cells in comparison to naturally occurring CD25 TR cells, we performed comparative gene expression profiling by Affymetrix microarray analysis. Sorted splenic wild-type (WT) TR cells, stg TR cells, dtg CD25-  TR cells, dtg CD25+  TR cells, in vitro-stimulated stg 16h TA cells, stg 3d TA cells as well as stg TN cells, were included in the experiment and analyses were performed in triplicates."'
GSE12506_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"To define the molecular signature of Ag-specific in vivo-induced dtg CD25 TR cells in comparison to naturally occurring CD25 TR cells, we performed comparative gene expression profiling by Affymetrix microarray analysis. Sorted splenic wild-type (WT) TR cells, stg TR cells, dtg CD25-  TR cells, dtg CD25+  TR cells, in vitro-stimulated stg 16h TA cells, stg 3d TA cells as well as stg TN cells, were included in the experiment and analyses were performed in triplicates."'
GSE12509_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Animals were injected i.p. 10mg/kg TCPOBOP or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the TCPOBOP treated ones and hybridized to Sterolgene V1 arrays."'
GSE12537_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Animals were injected i.p. 40mg/kg PCN or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the PCN treated ones and hybridized to Steroltalk V2 arrays."'
GSE12541-GPL2872_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"The mouse aldehyde oxidase, Aoh2 (aldehyde oxidase homolog 2), is a molybdo-flavoenzyme.  Harderian glands are the richest source of Aoh2, although  the protein is detectable also in sebaceous glands, epidermis and other keratinized epithelia.  The levels of Aoh2 in the Harderian gland and skin are controlled by genetic background, being maximal in CD1 or C57BL/6 and minimal in DBA/2, CBA or 129/Sv strains.  Testosterone is a negative regulator of Aoh2 in Harderian glands.  Homogenously purified Aoh2 oxidizes retinaldehyde into retinoic acid efficiently, while it is devoid of pyridoxal oxidizing activity, unlike other aldehyde oxidases.  Aoh2  knockout mice are viable and fertile, although they have an absolute deficit of retinaldehyde oxidase activity in the Harderian gland, decreased retinoic acid levels, and down-regulation of retinoid-dependent genes.  The Harderian gland’s transcriptome of knockout mice is characterized by perturbations in pathways controlling lipid homeostasis and cellular secretion.  This is particularly evident in sexually immature animals.  Lower amounts of retinoic acid are also observed in the skin of Aoh2-/- animals.  Knockout mice have thickening of the epidermis in basal conditions and after UV light exposure.  This has correlates in the skin transcriptome, which shows enrichment and overall up-regulation of genes involved in hypertrophic responses."'
GSE12541-GPL7202_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"The mouse aldehyde oxidase, Aoh2 (aldehyde oxidase homolog 2), is a molybdo-flavoenzyme.  Harderian glands are the richest source of Aoh2, although  the protein is detectable also in sebaceous glands, epidermis and other keratinized epithelia.  The levels of Aoh2 in the Harderian gland and skin are controlled by genetic background, being maximal in CD1 or C57BL/6 and minimal in DBA/2, CBA or 129/Sv strains.  Testosterone is a negative regulator of Aoh2 in Harderian glands.  Homogenously purified Aoh2 oxidizes retinaldehyde into retinoic acid efficiently, while it is devoid of pyridoxal oxidizing activity, unlike other aldehyde oxidases.  Aoh2  knockout mice are viable and fertile, although they have an absolute deficit of retinaldehyde oxidase activity in the Harderian gland, decreased retinoic acid levels, and down-regulation of retinoid-dependent genes.  The Harderian gland’s transcriptome of knockout mice is characterized by perturbations in pathways controlling lipid homeostasis and cellular secretion.  This is particularly evident in sexually immature animals.  Lower amounts of retinoic acid are also observed in the skin of Aoh2-/- animals.  Knockout mice have thickening of the epidermis in basal conditions and after UV light exposure.  This has correlates in the skin transcriptome, which shows enrichment and overall up-regulation of genes involved in hypertrophic responses."'
GSE12544_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The MYC oncogene has been implicated in the regulation of up to thousands of genes involved in many cellular programs including proliferation, growth, differentiation, self-renewal, and apoptosis. MYC is thought to induce cancer through an exaggerated effect on these physiologic programs. Which of these genes are responsible for the ability of MYC to initiate and/or maintain tumorigenesis is not clear. Previously, we have shown that upon brief MYC inactivation, some tumors undergo sustained regression. Here we demonstrate that upon MYC inactivation there are global permanent changes in gene expression detected by microarray analysis. By applying StepMiner analysis, we identified genes whose expression most strongly correlated with the ability of MYC to induce a neoplastic state. Notably, genes were identified that exhibited permanent changes in mRNA expression upon MYC inactivation. Importantly, permanent changes in gene expression could be shown by chromatin immunoprecipitation (ChIP) to be associated with permanent changes in the ability of MYC to bind to the promoter regions. Our list of candidate genes associated with tumor maintenance was further refined by comparing our analysis with other published results to generate a gene signature associated with MYC-induced tumorigenesis in mice. To validate the role of gene signatures associated with MYC in human tumorigenesis, we examined the expression of human homologs in 273 published human lymphoma microarray datasets in Affymetrix U133A format. One large functional group of these genes included the ribosomal structural proteins. In addition, we identified a group of genes involved in a diverse array of cellular functions including: BZW2, H2AFY, SFRS3, NAP1L1, NOLA2, UBE2D2, CCNG1, LIFR, FABP3, and EDG1. Hence, through our analysis of gene expression in murine tumor models and human lymphomas, we have identified a novel gene signature correlated with the ability of MYC to maintain tumorigenesis."'
GSE12544_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Compound Based Treatment: Bone tumor cells 1325 were treated/not treated with 20ng/ml of doxycycline"'
GSE12576_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Over-expression of wild type PrP in skeletal muscles is sufficient to cause a primary myopathy with no signs of peripheral neuropathy, possibly due to accumulation of a cytotoxic truncated form of PrP and/or PrP aggregation.  In this study we used DNA microarrays to identify 1499 transcripts that are temporally deregulated concomitant with inducible PrPC over-expression in the skeletal muscles of transgenic mice.  Examination using microarrays revealed a transcriptional profile with both similarities and differences to previously investigated models of myopathies.  Down-regulation of genes coding for the myofibrillar proteins MYH2, MYH6, MYH7, MYL2, MYL3 and up-regulation of lysosomal genes CTSS, CTSD, CTSZ, DPEP2, HEXA, HEXB and LAMP1 coincide with the observed myopathy and lysosome accumulation on over-expression of PrPC.  Down-regulation of the MEF2C gene, a key regulatory transcriptional factor muscle development and remodeling of adult muscles in response to physiologic and pathologic signals, may contribute to the centrally placed nuclei in the skeletal muscles.  Significantly, up-regulation of genes involved in p53 signaling and the induction of p53 protein, suggest a central role for this molecule in the myopathy.  Several p53-regulated genes involved in cell cycle arrest (CDNK1A, GADD45a and GADD45b) and apoptosis (BAK1, PMAIP1, BBC3, and BAX) are induced. We suggest that PrPC over-expression in skeletal muscles, possibly in response to accumulation of a cytotoxic truncated form of PrP, causes a primary myopathy involving the induction of p53-dependent pathways. "'
GSE12576_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Wild type (WT), PrP-null (KO), and Tg(HQK) mice were fed food pellets either lacking or containing 6g doxycycline (Dox)/kg food to induce PrPC expression. Skeletal muscles from the quadriceps of hind legs were removed at day 0, 4, 7, 14, 30 and 60 days following administration of Dox.  Total RNA was isolated from these tissues for use in subsequent microarray analysis. Mouse gene expression was analysed by two-colour microarray experiments using an inhouse manufactured 16K mouse cDNA microarray. Age matched reference mice (WT) and experimental (KO and HQK) Alexa Flour labeled aRNA were used in each competitive hybridization.  Each sample was labeled individually with both Alexa Fluor 555 and 647 for subsequent dye-swapped hybridizations to account for intensity bias. 3 individual mice from each experimental group at each time point were individually processed for separate microarrays.  We used the program EDGE to identify genes that were differentially expressed in mouse skeletal muscle in either transgenic HQK mice over expressing PrP, or PrP knock out (KO) mice  after administration of Dox.  We used a P value cut-off of 0.05 as the criteria of selection of significantly differentially expressed genes."'
GSE12581_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Gene expression profiles of the lymphoid and non-lymphoid leukemias induced by the Graffi murine leukemia retrovirus"'
GSE12591_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Angiotensin II induced aneurysms in male ApoE mice"'
GSE12599_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Transcriptional profiling of mouse glomerulus in lipopolysaccharide-induced proteinuria model"'
GSE12599_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"To gain insight into the pathogenesis of proteinuria development, we characterized the glomerular gene expression changes that accompany early stages of proteinuria induced by lipopolysaccharide (LPS) in mice."'
GSE12599_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Nine-week-old female C57Bl6 mice were  allocated to LPS-treated group (n=6) or PBS control group (n=4), and subsequently treated either by a single intraperitoneal injection LPS or control buffer."'
GSE12609_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"We have recently generated a transgenic mouse with a floxed Arx allele (Arxflox).  We have generated conditional knockouts in which Arx is removed specifically from the brain by mating Arxflox mice with transgenic mice expressing Cre behind the neural tube-specific transcriptional regulatory elements of the POU domain, class 3, transcription factor 4 promoter.  Preliminary analyses of these mice suggest that conditional knockout mice recapitulate the nonradial migration defects associated with conventional knockout mice.  We will compare the gene expression profiles of ganglion eminences (GEs; the anatomical source for nonradially migrating interneurons) from male Arxflox mice that express Pou3f-Cre to those from male mice without Arxflox allele.  Animals will be prepared and sacrificed following our institutional protocol.  Tissue will be rapidly dissected from E14.5 (the temporal peak of interneuron migration) GEs (MGE and LGE from both left and right hemispheres).  Preliminary experiments suggest that the amounts of RNA that can be isolated from a pair of GEs is in the range of 2000-3500 ng, which should be sufficient for microarray analysis following linear amplification of RNA.  The GEs from each animal will be combined, snap frozen in liquid nitrogen, and stored at -80 C until RNA is extracted.  Total RNA will be extracted using Trizol followed by RNA purification with the RNeasy cleanup kit.  We will be providing total RNA samples from four wildtype and four transgenic animals (true biological replicates) from three separate litters to mitigate any expression differences resulting from mouse to mouse or litter to litter variation."'
GSE12610_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Previous data by our lab and others have shown that neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) are upregulated under diabetic conditions in the retina.  Additional work in our lab has shown that the lack of  nitric oxide (NO) produced by nNOS may affect neurotransmitter production, particularly with GABA.  We have also shown that mice with induced diabetes show neurochemical changes in the retina after only one to three weeks.  Thus, we expect to see gene level changes associated with the retina before psysological changes in newly diabetic mice."'
GSE12618_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"FVB/N mice were time mated. At embryonic day 13 mice were euthanized by decapitation and the bladders were microdissected, cut just above the ureters, and treated with 20 µM EDTA for 20 minutes. Mesenchymal and epithelial compartments were then separated by rimming the bladder with a needle and harvested in RLT. Total RNA was isolated for gene expression analysis using the Affymetrix MOE430 microarray chip"'
GSE12628_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The infant leukemia-associated gene, Ott1(Rbm15), has broad regulatory effects within the murine hematopoiesis. However, germline Ott1 deletion  results in fetal demise prior to E10.5, indicating additional developmental requirements for Ott1. The spen gene family, to which Ott1 belongs, has a transcriptional activation/repression domain and RNA recognition motifs, and in Drosophila has a significant role in the development of the head and thorax. Early Ott1-deficient embryos show growth retardation and incomplete closure of the notochord. Further analysis demonstrated placental defects in the spongiotrophoblast and syncytiotrophoblast layers, resulting in an arrest of vascular branching morphogenesis. Rescue of the placental defect using a conditional allele with a trophoblast-sparing cre transgene allowed embryos to form a normal placenta and survive gestation. This result shows that the process of vascular branching morphogenesis in Ott1-deficient animals is regulated by the trophoblast compartment rather than the fetal vasculature. Mice surviving to term manifested hyposplenia and abnormal cardiac development. Analysis of global gene expression of Ott1-deficient embryonic hearts shows enrichment of hypoxia-related genes and significant alteration of several candidate genes critical for cardiac development. Thus, Ott1-dependent pathways in addition to being implicated in leukemogenesis, may also be important in the pathogenesis of placental insufficiency and cardiac malformations."'
GSE12628_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"RNA was extracted from 3 hearts each from  either Ott1null/nullSox2-cre or Ott1null/wtSox2-cre E18.5 embryos using the RNeasy Micro kit (Qiagen, Valencia, CA) and treated with RNAse-free DNAse (Qiagen, Valencia, CA). 50 ng of purified total RNA was linearly amplified using the Ovation RNA amplification system V2 (Nugen, San Carlos, CA) and biotinylated with the FL-Ovation Biotin Module V2 (Nugen, San Carlos, CA) per the supplied protocol. cDNA was then hybridized to Affymetrix Mouse expression array 430A2.0 chips by the Dana Farber Microarray Core Facility (Boston, MA).  The raw gene expression values were preprocessed with robust multi-array analysis (RMA) algorithm using BioConductor software."'
GSE12633_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"In the mouse neocortex, neural progenitor cells generate neurons through repeated rounds of asymmetric cell division. How distinct fates are established in their daughter cells is unclear. We show here that the TRIM-NHL protein TRIM32 segregates asymmetrically during progenitor division and induces neuronal differentiation in one of the two daughter cells. TRIM32 is highly expressed in differentiating neurons. In both horizontally and vertically dividing progenitor cells, TRIM32 distribution becomes polarized in mitosis so that the protein is enriched in one of the two daughter cells. While TRIM32 overexpression induces cell cycle exit and neuronal differentiation, TRIM32 RNAi causes both daughter cells to proliferate and prevents the initiation of a neuronal differentiation program . TRIM32 ubiquitinates and degrades the transcription factor c-Myc but also binds Argonaute-1 and thereby increases the activity of specific micro-RNAs. We show that Let-7 is one of the TRIM32 targets and is required and sufficient for neuronal differentiation. Our data suggest that the asymmetric segregation of a micro RNA regulator controls self renewal in the mammalian brain."'
GSE12673_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_title	"Whole heart response to stable HIF-1alpha overexpression"'
GSE12673_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Bi-allelic transgenic mice were created by crossing alpha-MHC promoter/tet transactivating protein expressing mice with tet responsive element promter/stable HIF-1alpha protein expressing mice.  Mice were either, maintained on Doxycycline (inhibiting the expression of the HIF-1alpha transgene) or removed from doxycycline (inducing expression) for one or three days."'
GSE12694_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"transcriptome comparisons of 2 independent p53-null with 3 p53/Pten double-null murine NSCs at 1 day post exposure to the differentiation inducer."'
GSE12697_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Trap-80-dependence of TNF-alpha-induced genes"'
GSE12697_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"RNA was extracted from three independent cultures of wild-type and Trap-80 knock-down fibroblasts, before and after stimulation for 1 hour with 5ng/ml TNF-alpha.  The unstimulated and stimulated wild-type samples, and the stimulated Trap-80 knock-down samples, were used for microarray analysis."'
GSE12716_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Differential gene expression in mice liver after apigenin administration. Gene expression from control mice were compared with apigenin treated mice at different dose level."'
GSE12836_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We analyzed the generation of mouse gliomas following the overexpression of PDGF-B in embryonic neural progenitors. Comparison of our microarray data, with published gene expression data sets for many different murine neural cell types, revealed a closest relationship between our tumor cells and oligodendrocyte progenitor cells, confirming definitively that PDGF-B-induced gliomas are pure oligodendrogliomas."'
GSE12836_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"We analyzed the generation of mouse gliomas following the overexpression of PDGF-B in embryonic neural progenitors. Comparison of our microarray data, with published gene expression data sets for many different murine neural cell types, revealed a closest relationship between our tumor cells and oligodendrocyte progenitor cells, confirming definitively that PDGF-B-induced gliomas are pure oligodendrogliomas."'
GSE12847_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Col1a1 is located on mouse distal chromosome 11 (Celera 94607393-94622990bp; 15kb) and encodes type I procollagen that associates stoichiometrically with col1a2 in forming secreted type I mature collagen that self-assembles into a supramolecular fibrillar structure consisting of a protein family. Type I collagens are predominantly enriched in bone, cartilage, skin, tendons, and eye (i.e. in major fibrous tissues) making up the main extracellular matrix (ECM) component for support and scaffolding purposes. Col1a1 is known to be expressed in the embryo (E9.5; Northern dot blot), perioptic mesenchyme (E11), cornea (E11), skeleton (E14.5), brain meninges (E14.5), and cartilage (E14.5) at relatively early stages. Most evidence of type I collagen function is coupled to the latter stages of skeletal development, thus bypassing the major events of axis formation, tissue differentiation, and mesenchlymal-epithial interactions, for example, that are more symbolic of morphogens and growth factors. Members of the integrin cell surface receptor family of molecules mediate cell adhesion to ECM proteins such as collagen (mainly to type IV basement membrane collagen that forms into a polygonal meshwork), fibronectin, and laminin implicated in wound healing and inflammatory responses (e.g. Crohn disease, ulcerative colitis) in connective tissues. There is some evidence for protein-protein interactions between leukocyte-associated integrins and the interstitial matrix in promoting the migration and/or activation of extravasated leukocytes (e.g., T cells and monocytes) within the perivascular compartment, an ECM-rich environment. This region is surmised to be an important location where certain human leukocytes undergo differentiation (e.g. monocytes) and activation (neutrophils, monocytes, lymphocytes) upon extravascular migration. The von Willebrand factor (vWF), type C motif is found in various plasma proteins like complement factors, the integrins, collagen types, and other extracellular proteins. Thus, the majority of vWF-containing proteins are extracellular and a common feature appears to be involvement in multi protein complexes participating in numerous biological events (e.g. cell adhesion, migration, homing, pattern formation, and signal transduction)."'
GSE12863_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Breast TAMs were isolated from early-stage PyMT-induced mammary tumors expressing Ets2 and also from the tumors with Ets2-deficient TAMs. Since macrophages have also been implicated in normal mammary gland remodeling, normal remeodeling macrophages were also purified from females expressing Ets2 and the ones where Ets2 is deleted in the macrophages. One RNA sample was extracted from each genetic group for gene-expression profiling."'
GSE12863_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Breast TAMs were isolated from early-stage PyMT-induced mammary tumors expressing Ets2 and also from the tumors with Ets2-deficient TAMs. Since macrophages have also been implicated in normal mammary gland remodeling, normal remeodeling macrophages were also purified from females expressing Ets2 and the ones where Ets2 is deleted in the macrophages. One RNA sample was extracted from each genetic group for gene-expression profiling."'
GSE12929_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"3T3-L1 (Pre-adipocyte) cell line was induced to differentiate using standard adipocyte differentiation media (IBMX, Dex and Insulin) 48hrs post-confluency. RNA was harvested at day -2 (confluent fibroblasts), 48hrs post-induction with IBMX, DEX and Insulin (day=0) and for each subsequent day after rosiglitazone treatment. Illumina beadchip microarrays were used to determine expression profiles of genes differentially regulated in cells transfected with either siRNA targeting PPARgamma or a non-targeting control siRNA."'
GSE12929_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"3T3L1 cell were induced to differentiate into adipocytes using IBMX, DEX and Insulin. RNA from cell treated with PPARg-specific siRNA and non-specific siRNA was isolated at different timepoints. Illumina MouseRef-8 v1.1 Bead chips were used for expression profiling"'
GSE12929_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"3T3L1 cell were induced to differentiate into adipocytes using IBMX, DEX and Insulin. RNA from cell treated with PPARg-specific siRNA and non-specific siRNA was isolated at different timepoints. Illumina MouseRef-8 v1.1 Bead chips were used for expression profiling"'
GSE12948_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Oncogenesis of T-ALL and non-malignant consequences of overexpressing NOTCH1"'
GSE12948_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"We have determined the consequences of ICN1 overexpression from retroviral vectors introduced into bone marrow cells. "'
GSE12949_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_title	"GBM Xenograft response to 1 hour and 8 hour Cilengitide exposure"'
GSE12949_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"4 replicates of mice brains with tumor 103 are used as a control for expression with no cilengtide exposure.  4 replicates of mice brains with tumor 104 were exposed to cilengitide for 1 hour.  4 replicates of mice brains with tumor 105 were exposed to cilengitide for 8 hours."'
GSE12950_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Cryptorchidism and scrotal heating result in abnormal spermatogenesis but the mechanism(s) proscribing this temperature sensitivity are unknown.  It was previously reported that the AKR/N or MRL/MpJ-+/+ mouse testis is more heat resistant than the testis from the C57BL/6 strain.  We have attempted to probe into the mechanism(s) involved in heat sensitivity by examining global gene expression profiles of normal and heat-treated testes from C57BL/6, AKR/N and MRL/MpJ-+/+ mice by microarray analysis.  In the normal C57BL/6 testis, 415 and 416 transcripts were differentially expressed (at least two-fold higher or lower) when compared to the normal AKR/N and MRL/MpJ-+/+ testis, respectively.  The AKR/N and MRL/MpJ-+/+ strains revealed 268 differentially expressed transcripts between them.  There were 231 transcripts differentially expressed between C57BL/6 and two purported heat-resistant strains, AKR/N and MRL/MpJ-+/+."'
GSE12957_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"""Triggering TLR7 in mice induces immune activation and lymphoid system disruption, resembling HIV-mediated pathology"", Baenziger et al. Blood 2008"'
GSE12957_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mice (n=3/sample) were treated with 1mg/kg/d R848 or PBS (Mock) for 7 days. Thereafter, spleen was removed, mRNA extracted from whole splenic tissue and subsequently subjected to microarray RT² Profiler PCR array (Bioscience Corporation) on a Biorad iCycler. The PCR Array system examines the expression of 84 genes related to TLR-mediated signal transduction. "'
GSE12957_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"The supplementary file show data generated by real-time quantitative PCR normalized to Hypoxanthine guanine phosphoribosyl transferase 1, Heat shock protein 90kDa alpha, and Glyceraldehyde-3-phosphate dehydrogenase, displayed as fold difference in the expression of each gene between R848- and Mock-treated samples. Two independent experiments are summarized for wild-type mice. TLR7- and IFNAR-/- animals were tested once."'
GSE12986_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"a fusion construct of either Cdx2 or Gata3 and the tamoxifen responsive estrogen receptor ligand binding domain was expressed in R1 ES cells. Cell were induced with tamoxifen for 6 days to activate the transcription factor and cultured under trophoblast stem cell conditions"'
GSE12993_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"To predict Rp58-regulated gene involved in myogenesis, RNA profiling experiments were performed, comparing RNA derived from C2C12 with or without expressing shRNA for Rp58. As a result, 271 genes were upregulated in C2C12 stably expressing shRNA-Rp58 cells compared with control C2C12 cells. As Rp58 is repressor in C2C12, we hypothesized that Rp58 regulates gene cluster which expression is downregulated in accordance with Rp58 expression and myogenesis progression. In this regard, we also characterized dynamic gene expression patterns during myogenesis by microarray at 4 different stage (GM, day 0, 2, 4) of C2C12 myogenesis assays and found that 399 genes expression is characterized as downregulation pattern during myogenesis. Importantly, this down regulation gene set and upregulated genes by shRNA for Rp58 were highly overlapped."'
GSE12999_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"The first lineage decisions during mouse development lead to establishment of embryonic and extraembryonic tissues. The transcription factor Cdx2 plays a central role by repressing pluripotency genes, such as Oct4 and promoting trophoblast fate at the blastocyst stage. Here we show that the transcription factor Gata3 is coexpressed with Cdx2 in the blastocyst and that overexpression of Gata3 in embryonic stem cells is sufficient to induce expression of trophoblast genes. Gata3 expression in the blastocyst does not depend on Cdx2, nor do Gata3 overexpressing cell lines require Cdx2 for expression of a subset of trophoblast genes. In the embryo, expression of Gata3, like Cdx2, depends on Tead4, and expression of both factors becomes restricted to nascent trophoblast by an Oct4-independent mechanism. These observations place Tead4 at the top of a trophoblast hierarchy, with Gata3 and Cdx2 acting downstream to induce expression of common and independent targets in this lineage."'
GSE12999_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"The first lineage decisions during mouse development lead to establishment of embryonic and extraembryonic tissues. The transcription factor Cdx2 plays a central role by repressing pluripotency genes, such as Oct4 and promoting trophoblast fate at the blastocyst stage. Here we show that the transcription factor Gata3 is coexpressed with Cdx2 in the blastocyst and that overexpression of Gata3 in embryonic stem cells is sufficient to induce expression of trophoblast genes. Gata3 expression in the blastocyst does not depend on Cdx2, nor do Gata3 overexpressing cell lines require Cdx2 for expression of a subset of trophoblast genes. In the embryo, expression of Gata3, like Cdx2, depends on Tead4, and expression of both factors becomes restricted to nascent trophoblast by an Oct4-independent mechanism. These observations place Tead4 at the top of a trophoblast hierarchy, with Gata3 and Cdx2 acting downstream to induce expression of common and independent targets in this lineage."'
GSE13005_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Using a macrophage cell line, we demonstrate the ability of amorphous silica particles to stimulate inflammatory protein secretion and induce cytotoxicity.  Whole genome microarray analysis of early gene expression changes induced by 10nm and 500nm particles showed that the magnitude of change for the majority of genes correlated more tightly with particle surface area than either particle mass or number.  Gene expression changes that were size-specific were also identified, however the overall biological processes represented by all gene expression changes were nearly identical, irrespective of particle diameter.  Our results suggest that on an equivalent nominal surface area basis, common biological modes of action are expected for nano- and supranano-sized silica particles."'
GSE13005_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"RAW 264.7 mouse macrophage cells were treated with two sizes of amorphous silica particles at three doses each for 2 hours.  Cells were exposed to 10nm silica at 5 (low), 20 (mid), or 50 (high) ug/ml or 500nm silica at 250 (low), 500 (mid), or 1000 (high) ug/ml in serum-free medium."'
GSE13010_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Cryptorchidism and scrotal heating result in abnormal spermatogenesis but the mechanism(s) proscribing this temperature sensitivity are unknown.  It was previously reported that the AKR/N or MRL/MpJ-+/+ mouse testis is more heat resistant than the testis from the C57BL/6 strain.  We have attempted to probe into the mechanism(s) involved in heat sensitivity by examining global gene expression profiles of normal and heat-treated testes from C57BL/6, AKR/N and MRL/MpJ-+/+ mice by microarray analysis.  In the normal C57BL/6 testis, 415 and 416 transcripts were differentially expressed (at least two-fold higher or lower) when compared to the normal AKR/N and MRL/MpJ-+/+ testis, respectively.  The AKR/N and MRL/MpJ-+/+ strains revealed 268 differentially expressed transcripts between them.  There were 231 transcripts differentially expressed between C57BL/6 and two purported heat-resistant strains, AKR/N and MRL/MpJ-+/+.  Next, the testes of C57BL/6 and AKR/N mice were exposed to 43ºC for 15 min and harvested at different time points for TUNEL studies and microarrays.  An increase of TUNEL-positive germ cell numbers was significant 8 hr after heat exposure in the C57BL/6 mouse.  However, this increase was not observed in the AKR/N mouse until 10 hr after heat exposure.  All tubules showed germ cell loss and disruption in C57BL/6 testis 24 hr after heat shock.  In contrast, although a number of seminiferous tubules showed an abnormal morphology 24 hr post-heat shock in the AKR/N mouse, many tubules still retained a normal structure.  Numerous transcripts exhibited differential regulation between the two strains within 24 hours after heat exposure.  The differentially expressed transcripts in the testes 8 hr after heat exposure were targeted to identify the genes involved in the initial response rather than those due to germ cell loss.  Twenty transcripts were significantly down-regulated and 19 genes were up-regulated by hyperthermia in C57BL/6 and did not show a parallel change in the AKR/N testis.  Conversely, heat shock resulted in 30 up-regulated transcripts and 31 down-regulated transcripts in AKR/N that were not similarly regulated in C57BL/6.  A number of genes shared similar differential expression patterns and differential regulation by hyperthermia in both strains of mice.  Taken together, the present study indicates the diverse genetic backgrounds in the three strains lead to major differences in normal testis gene expression profiles while the differences in heat shock responses involves a significantly smaller number of genes.  The data generated may provide insights regarding gene networks and pathways involved in heat stress and their relationship to spermatogenesis.  "'
GSE13010_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Cryptorchidism and scrotal heating result in abnormal spermatogenesis but the mechanism(s) proscribing this temperature sensitivity are unknown.  It was previously reported that the AKR/N or MRL/MpJ-+/+ mouse testis is more heat resistant than the testis from the C57BL/6 strain.  We have attempted to probe into the mechanism(s) involved in heat sensitivity by examining global gene expression profiles of normal and heat-treated testes from C57BL/6, AKR/N and MRL/MpJ-+/+ mice by microarray analysis.  In the normal C57BL/6 testis, 415 and 416 transcripts were differentially expressed (at least two-fold higher or lower) when compared to the normal AKR/N and MRL/MpJ-+/+ testis, respectively.  The AKR/N and MRL/MpJ-+/+ strains revealed 268 differentially expressed transcripts between them.  There were 231 transcripts differentially expressed between C57BL/6 and two purported heat-resistant strains, AKR/N and MRL/MpJ-+/+.  Next, the testes of C57BL/6 and AKR/N mice were exposed to 43ºC for 15 min and harvested at different time points for TUNEL studies and microarrays.  An increase of TUNEL-positive germ cell numbers was significant 8 hr after heat exposure in the C57BL/6 mouse.  However, this increase was not observed in the AKR/N mouse until 10 hr after heat exposure.  All tubules showed germ cell loss and disruption in C57BL/6 testis 24 hr after heat shock.  In contrast, although a number of seminiferous tubules showed an abnormal morphology 24 hr post-heat shock in the AKR/N mouse, many tubules still retained a normal structure.  Numerous transcripts exhibited differential regulation between the two strains within 24 hours after heat exposure.  The differentially expressed transcripts in the testes 8 hr after heat exposure were targeted to identify the genes involved in the initial response rather than those due to germ cell loss.  Twenty transcripts were significantly down-regulated and 19 genes were up-regulated by hyperthermia in C57BL/6 and did not show a parallel change in the AKR/N testis.  Conversely, heat shock resulted in 30 up-regulated transcripts and 31 down-regulated transcripts in AKR/N that were not similarly regulated in C57BL/6.  A number of genes shared similar differential expression patterns and differential regulation by hyperthermia in both strains of mice.  Taken together, the present study indicates the diverse genetic backgrounds in the three strains lead to major differences in normal testis gene expression profiles while the differences in heat shock responses involves a significantly smaller number of genes.  The data generated may provide insights regarding gene networks and pathways involved in heat stress and their relationship to spermatogenesis.  "'
GSE13010_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Total RNA of testes from two different strains of mice, C57BL/6 and AKR/N were analyzed using microarray 430.20 chip.  Duplicates were used in controls and treated samples at 8hr, 10hr, 12hr, 24hr after heat shock at 43C for 15 min.  All mice were 8 weeks old."'
GSE13031_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways."'
GSE13031_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways."'
GSE13031_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways."'
GSE13031_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways."'
GSE13032_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Resiquimod is a nucleoside analog belonging to the imidazoquinoline family of compounds which is known to signal through Toll-like receptor 7.  Resiquimod treatment has been demonstrated to inhibit the development of allergen induced asthma in experimental models.  Despite this demonstrated effectiveness, little is known about the molecular events responsible for this effect.  The aim of the present study was to elucidate the molecular processes which were altered following resiquimod treatment and antigen challenge in a mouse model of allergic asthma.  Employing microarray analysis, we have characterized the “asthmatic” transcriptome of the murine lung and determined that it includes genes involved in: the control of cell cycle progression, airway remodelling, the complement and coagulation cascades, and chemokine signalling.  We have demonstrated that systemic resiquimod administration resulted in the recruitment of NK cells to the lungs of the mice, although no causal relationship between NK cell recruitment and treatment efficacy was found.  Furthermore, results of our studies demonstrated that resiquimod treatment resulted in the normalization of the expression of genes involved with airway remodelling and chemokine signalling, and in the modulation of the expression of genes including cytokines and chemokines, adhesion molecules, and B-cell related genes, involved in several aspects of immune function and antigen presentation.  Overall, our findings identified several genes, important in the development of asthma pathology, that were normalized following resiquimod treatment thus improving our understanding of the molecular consequences of resiquimod treatment in the lung milieu."'
GSE13035-GPL1261_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"Mitochondrial dysfunction by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response"'
GSE13035-GPL339_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"Mitochondrial dysfunction by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response"'
GSE13044_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Exposure to PFOA during gestation altered the expression of genes related to fatty acid catabolism in both the fetal liver and lung.  In the fetal liver, the effects of PFOA were robust and also included genes associated with lipid transport, ketogenesis, glucose metabolism, lipoprotein metabolism, cholesterol biosynthesis, steroid metabolism, bile acid biosynthesis, phospholipid metabolism, retinol metabolism, proteosome activation, and inflammation.  These changes are consistent with activation of PPAR alpha.  Non-PPAR alpha related changes were suggested as well."'
GSE13071_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Knee joint synovium from different grades of inflammation in mouse collagen induced arthritis (CIA)"'
GSE13071_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Knee joint synovium was used for gene expression analysis of mouse collagen induced arthritis (CIA).  Synovium was prepared at day 30 after initial sensitization from: healthy controls, CIA animals with no, with mild, with moderate, or with severe joint inflammation.  Each sample group is represented by three replicates, each consisting of tissue collected from three to four animals."'
GSE13075_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"ES cells were left untreated or treated with 2 mM H2O2 for 1 hour. Both samples were subjected to ChIP against SIRT1, H1AcK26 or rabbit Ig (one IP per treatment and Ab). Input DNA was labeled with Cy3, IP DNA with Cy5, enrichment over input is reported as 2log."'
GSE13106_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Murine 6dpp Sertoli Cell treated with 0ng, 5ng, 50ng activin (duplicates). "'
GSE13106_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Murine 15dpp Sertoli Cell treated with 0ng, 5ng activin (duplicates). Total 10 samples."'
GSE13125-GPL1261_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"PU.1 is a key transcription factor for macrophage differentiation. Novel PU.1 target genes were identified by mRNA profiling of PU.1-deficient progenitor cells (PUER) before and after PU.1 activation. We used two different types of Affymetrix DNA-microarrays (430 2.0 arrays and ST 1.0 exon arrays) to characterize the global PU.1-regulated transcriptional program underlying the early processes of macrophage differentiation."'
GSE13125-GPL1261_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Uninduced and 24h 4-hydroxy-tamoxifen (OHT) induced PUER cells were cultured before RNA extraction and hybridization on Affymetrix Mouse Genome 430 2.0 and Mouse Exon ST 1.0 microarrays. Triplicates before (0h) and after (24h) induction of PU.1 were analyzed."'
GSE13125-GPL6096_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"PU.1 is a key transcription factor for macrophage differentiation. Novel PU.1 target genes were identified by mRNA profiling of PU.1-deficient progenitor cells (PUER) before and after PU.1 activation. We used two different types of Affymetrix DNA-microarrays (430 2.0 arrays and ST 1.0 exon arrays) to characterize the global PU.1-regulated transcriptional program underlying the early processes of macrophage differentiation."'
GSE13125-GPL6096_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Uninduced and 24h 4-hydroxy-tamoxifen (OHT) induced PUER cells were cultured before RNA extraction and hybridization on Affymetrix Mouse Genome 430 2.0 and Mouse Exon ST 1.0 microarrays. Triplicates before (0h) and after (24h) induction of PU.1 were analyzed."'
GSE13129_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We wished to examine the genes regulated by FoxD3 in pigment cells to gain understanding in how FoxD3 represses melanoblast specification in the neural crest.  For technical reasons, we could not use neural crest cells, so we used melanoma cells, since they are derived from neural crest cells.  To this end, we transfected B16-F10 mouse melanoma cells with constructs expressing FoxD3, or FoxD3-VP16, in which the C-terminal portion of FoxD3 (which contains the transcriptional repression domain) has been replaced by the VP16 transcriptional activation domain."'
GSE13129_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"We wished to examine the genes regulated by FoxD3 in pigment cells to gain understanding in how FoxD3 represses melanoblast specification in the neural crest.  For technical reasons, we could not use neural crest cells, so we used melanoma cells, since they are derived from neural crest cells.  To this end, we transfected B16-F10 mouse melanoma cells with constructs expressing FoxD3, or FoxD3-VP16, in which the C-terminal portion of FoxD3 (which contains the transcriptional repression domain) has been replaced by the VP16 transcriptional activation domain."'
GSE13129_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_overall_design	"B16-F10 cells were transfected with either empty pMES, pFoxD3 (which contains FoxD3 inserted into pMES), or pFoxD3-VP16 (similar to pFoxD3, except that the C-terminal portion of FoxD3, which contains the transcriptional repression domain, has been replaced by the transcriptional activation domain of VP16)."'
GSE13130_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The arylhydrocarbon receptor is a ligand inducible transcription factor. Known to control xenobiotic metabolizing enzymes, it also affects - depending on the cell type - numerous other genes, either directly or indirectly. With respect to the immune system, persistent activation leads to immunosuppression. We asked how the AhR is involved in Langerhans cells. These antigen presenting cells of the skin are responsible for allergies against chemicals (thus xenobiotic metabolism might be relevant) and a recently detected endogenous ligand, FICZ made by UVB radiation from tryptophane, is particularly abundant in the skin."'
GSE13140_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"DAP12 is a transmembrane protein, expressed as a disulfide-bonded homodimer and bears an immunoreceptor tyrosine-based activation motif (ITAM). DAP12 is broadly expressed in hematopoietic cells and associates with a variety of cell surface receptors in lymphoid and myeloid cells. Macrophages express several DAP12-associated receptors including triggering receptors expressed by myeloid cells (TREM)-1,2 and 3, myeloid DAP12-associating lectin (MDL)-1, CD200R like proteins CD200R3/R4 and CD300C/D/E ."'
GSE13148_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In the present microarray study, we set out to identify age- and arthritis-related gene expression pattern changes in proteoglycan (aggrecan)-induced arthritis (PGIA) model."'
GSE13156_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"As the Crh-system and the HPA-axis are known to be crucially involved in the onset, development and maintainance of psychiatric disorders like anxiety and depression and regulate the behavioural and endocrine stress responses the further analysis of Crhr1-dependent signaling cascades is essential to understand the molecular mechanisms behind these psychiatric diseases. In this project, new candidate genes involved in Crhr1-dependent signaling cascades were dissected in the cell line model of AtT-20 cells by transcriptional profiling of mouse pituitary corticotroph cells comparing control untreated AtT-20 cells with AtT-20 cells treated with 100 nM Crh at 1, 3, 6, 12 and 24 hours."'
GSE13156_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Two condition experiment: untreated vs. 100 nM Crh treated AtT-20 cells with a time curve of 1, 3, 6, 12, 24 hours. Technical replicates: 6 for each time point, including dye-swap each with 3 replicates"'
GSE13160_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"By means of Operon V3 microarrrays, the in vivo, aortic endothelial transcriptomic responses to chronic (30 day) whole body exposure to diesel exhaust were assessed in wild type and Apo E (-/-) mice.  The in vitro response of cultured Svec 4-10 cells exposed  to a soluble extract extract of diesel engine particulate were similarly assessed."'
GSE13160_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"Mice of the Tie 2 GFP strain as well as a stable hybrid strain derived by cross of Tie 2 GFP with the Apo E (-/-) strain were bred in suffficient quantities for these experiments.  Male mice at 4 months of age at the initiation of the exposure to 30 days of dilute diesel engine 94 hours/day, 5 days/week) at either 0 (control), 300 or 1000 ug/ cubic meter exhaust particulate.   Following exposure, three pooled aortae of each experimental and ceach c age-matched control group were dissected from the aortic arch to the iliac bifurcation, minced and collagenolytically digested prior to FACS into Trizol.  Purification yielded aortic endothelial RNA subjected to amplification with Nugen isothermal linear amplification to produce amplified cDNA.  Microarrays were performed with a single dye reversal to compare the transcriptome of exposed mice to age-matched control mice.  "'
GSE13189_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Expression of meningioma 1 (MN1) has been proposed to be a negative prognostic molecular marker in adult AML with normal cytogenetics, however its role in pediatric leukemia is unknown. We found elevated MN1 expression in 53 of 88 pediatric leukemia cases: significant amounts of MN1 were found in immature B-cell ALL and most cases of infant leukemia but no MN1 expression was detected in T-cell acute lymphoblastic leukemia (T-ALL). Interestingly 17 of 19 cases harboring MLL-X fusions showed also elevated MN1 expression. Lentiviral siRNA mediated MN1 knock-down resulted in cell cycle arrest and impaired clonogenic growth of 3 MLL-X-positive human leukemia cell lines overexpressing MN1 (THP-1, RS4;11, MOLM13). In a mouse MLL/ENL-induced leukemia MN1 overexpression resulted from retroviral provirus insertion. Strikingly co-expression of MN1 with MLL/ENL resulted in significantly reduced latency for induction of an AML phenotype in mice suggesting functional cooperation. MN1 overexpression in MLL/ENL-carrying cells resulted in expansion of the L-GMP population and facilitated disease induction in secondary recipients. Gene expression profiling allowed to define a number of potential MN1 hematopoietic targets. Up-regulation of CD34, FLT3, HLF, or DLK1 was validated in bone marrow transiently overexpressing MN1, in MN1-induced mouse leukemias, as well as in some cases of pediatric leukemias overexpressing MN1. Taken together, our work suggests that MN1 overexpression is essential for growth of leukemic cells, and that MN1 can act as a cooperating oncogene with MLL-X fusion genes most probably through modification of a distinct gene expression program that leads to expansion of a leukemia initiating cell population. "'
GSE13189_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"Expression of meningioma 1 (MN1) has been proposed to be a negative prognostic molecular marker in adult AML with normal cytogenetics, however its role in pediatric leukemia is unknown. We found elevated MN1 expression in 53 of 88 pediatric leukemia cases: significant amounts of MN1 were found in immature B-cell ALL and most cases of infant leukemia but no MN1 expression was detected in T-cell acute lymphoblastic leukemia (T-ALL). Interestingly 17 of 19 cases harboring MLL-X fusions showed also elevated MN1 expression. Lentiviral siRNA mediated MN1 knock-down resulted in cell cycle arrest and impaired clonogenic growth of 3 MLL-X-positive human leukemia cell lines overexpressing MN1 (THP-1, RS4;11, MOLM13). In a mouse MLL/ENL-induced leukemia MN1 overexpression resulted from retroviral provirus insertion. Strikingly co-expression of MN1 with MLL/ENL resulted in significantly reduced latency for induction of an AML phenotype in mice suggesting functional cooperation. MN1 overexpression in MLL/ENL-carrying cells resulted in expansion of the L-GMP population and facilitated disease induction in secondary recipients. Gene expression profiling allowed to define a number of potential MN1 hematopoietic targets. Up-regulation of CD34, FLT3, HLF, or DLK1 was validated in bone marrow transiently overexpressing MN1, in MN1-induced mouse leukemias, as well as in some cases of pediatric leukemias overexpressing MN1. Taken together, our work suggests that MN1 overexpression is essential for growth of leukemic cells, and that MN1 can act as a cooperating oncogene with MLL-X fusion genes most probably through modification of a distinct gene expression program that leads to expansion of a leukemia initiating cell population. "'
GSE13189_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Expression of meningioma 1 (MN1) has been proposed to be a negative prognostic molecular marker in adult AML with normal cytogenetics, however its role in pediatric leukemia is unknown. We found elevated MN1 expression in 53 of 88 pediatric leukemia cases: significant amounts of MN1 were found in immature B-cell ALL and most cases of infant leukemia but no MN1 expression was detected in T-cell acute lymphoblastic leukemia (T-ALL). Interestingly 17 of 19 cases harboring MLL-X fusions showed also elevated MN1 expression. Lentiviral siRNA mediated MN1 knock-down resulted in cell cycle arrest and impaired clonogenic growth of 3 MLL-X-positive human leukemia cell lines overexpressing MN1 (THP-1, RS4;11, MOLM13). In a mouse MLL/ENL-induced leukemia MN1 overexpression resulted from retroviral provirus insertion. Strikingly co-expression of MN1 with MLL/ENL resulted in significantly reduced latency for induction of an AML phenotype in mice suggesting functional cooperation. MN1 overexpression in MLL/ENL-carrying cells resulted in expansion of the L-GMP population and facilitated disease induction in secondary recipients. Gene expression profiling allowed to define a number of potential MN1 hematopoietic targets. Up-regulation of CD34, FLT3, HLF, or DLK1 was validated in bone marrow transiently overexpressing MN1, in MN1-induced mouse leukemias, as well as in some cases of pediatric leukemias overexpressing MN1. Taken together, our work suggests that MN1 overexpression is essential for growth of leukemic cells, and that MN1 can act as a cooperating oncogene with MLL-X fusion genes most probably through modification of a distinct gene expression program that leads to expansion of a leukemia initiating cell population. "'
GSE13190_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming."'
GSE13192_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Liver X receptors (LXRs) are important regulators of cholesterol, lipid and glucose metabolism and have been extensively studied in liver, macrophages and adipose tissue. However, their role in skeletal muscle is not yet fully elucidated and the functional role of each of the LXRα and LXRβ subtypes in skeletal muscle is at present unknown. To study the importance of each of the receptor subtypes, myotube cultures derived from wild type (WT), LXRα and LXRβ knockout (KO) mice were established. The present study shows that treatment with the unselective LXR agonist T0901317 increased mRNA levels of LXR target genes such as sterol regulatory element-binding transcription factor 1 (SREBF1), fatty acid synthase (FASN), stearoyl-CoA desaturase 1 (SCD1) and ATP-binding cassette transporter A1 (ABCA1) in myotubes established from WT and LXRα KO mice. However, only minor changes in expression level were observed for these genes after treatment with T0901317 in myotubes from LXRβ KO mice. Gene expression analysis using Affymetrix NuGO Genechip arrays showed that few other genes than the classical, well known LXR target genes were regulated by LXR in skeletal muscle. Furthermore, functional studies using radiolabeled substrates showed that treatment with T0901317 increased lipogenesis and apoA1 dependent cholesterol efflux, in myotubes from WT and LXRα KO mice, but not LXRβ KO mice. The data suggest that the lipogenic effects of LXRs, as well as the LXR-stimulated cholesterol efflux, are mainly mediated by LXRβ in skeletal muscle."'
GSE13192_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"To study the importance of each of the receptor subtypes, myotube cultures derived from wild type (WT), LXRa and LXRb knockout (KO) mice were established. Sixteen samples were examined. Half the samples were treated with the unselective LXR agonist T0901317."'
GSE13207_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We completed genome-wide microarray analysis in Sirt6 knockout (ko) mouse embryonic fibroblasts (MEFs) and control wildtype (wt) MEFs. Prior to RNA extraction, MEFs were treated with TNF-alpha (10 ng/ml) for the indicated times. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Ambion Amino Allyl MessageAmp II Amplification kit. Amplified mouse Universal Reference RNA (Stratagene) was used as reference RNA for analysis. Array hybridization of mouse MEEBO arrays is as described (Hendrickson et al., PLoS ONE, 2008)."'
GSE13211_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming."'
GSE13212_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming."'
GSE13235_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"In order to identify the genes regulated in mouse embryonic stem cells (mESC) by the effect of low concentrations of nitric oxide (NO), we analysed the transcriptome of cells treated with NO and compared it to those of cells cultured in the absence of leukemia inhibitory factor (LIF), and in the presence of LIF. We used the cell line D3-pOct4, which carries the enhanced Green Fluorescence Protein gene (eGFP) under the control of the Oct-4 promotor. This line is continuously maintained in the undifferentiated state in the presence of LIF, in comparison with the wild type line ."'
GSE13237_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily.  OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis.  METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP.  RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome.  CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis."'
GSE13237_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily.  OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis.  METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP.  RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome.  CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis."'
GSE13237_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"two condition experiment, Sertoli cells-rich areas from DEHP-treated mice vs. Sertoli cells-rich areas from vehicle-treated mice. Biological replicates: 4 DEHP-treated samples and 4 vehicle-treated samples. Dye-swap design. N=4 DEHP-treated vs vehicle-treated x 2 microarrays (dye-swap)=8 microarrays"'
GSE13240_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily.  OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis.  METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP.  RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome.  CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis."'
GSE13240_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily.  OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis.  METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP.  RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome.  CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis."'
GSE13240_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"two condition experiment, Leydig cells from DEHP-treated mice vs. Leydig cells from vehicle-treated mice. Biological replicates: 2 DEHP-treated samples and 3 vehicle-treated samples. Each treated sample has been hybridized against each vehicle-treated sample in a dye-swap design. N=2 DEHP-treated x 3 vehicle-treated x 2 microarrays=12 microarrays"'
GSE13243_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Recent improvements in the development of methods for isolating functionally validated populations of nearly pure (>20%) murine hematopoietic stem cells (HSCs) have made it possible to analyze the molecular basis of the properties of these cells with increased precision. One intriguing feature of HSCs is the change they undergo in many of their key properties during development a change that affects the control of their self-renewal, cycling status, differentiated progeny output and steel factor sensitivity. To investigate how these differences are mediated, we undertook a genome-wide analysis of the transcripts present in highly purified fetal and adult HSCs using an adaptation of the LongSAGE methodology that allows its application to small numbers of cells (10 ng of RNA) by inclusion of an initial PCR amplification step that preserves the transcript repertoire while excluding less than 0.25% of the transcripts. The LongSAGE methodology was adopted because it is sequence-based and thus quantitative and independent of prior knowledge of expressed genes or variations in their hybridization to matching or related cDNAs, ESTs or derived oligos. A suspension of 10,000 lin-Sca-1+CD43+Mac1+ fetal liver (FL) cells (20% pure HSCs as determined by 16-week limiting dilution and single cell transplantation experiments) was obtained from embryonic day 14.5 fetuses. From these cells, we generated a 160,000-tag LongSAGE library containing 7865 tags that map uniquely to the mouse genome (using the RefSeq database through DiscoverySpace; www.bcgsc.ca/DiscoverySpace). A suspension of 3700 CD45midlin-Rho-SP cells (30% pure HSCs) was isolated from adult mouse bone marrow (BM) and then used to generate a 37,000-tag LongSAGE library (956 uniquely mapped tags). Both of these libraries contained tags identifying transcripts that have been previously reported to be associated with HSCs from FL and/or adult BM, including c-kit, pbx-1, tgf-, cul-4a, PrP, c-myc, robo1, sox17, as well as a number of Smarc transcripts, ubiquitin ligase transcripts and TNF-related transcripts. As a first test of the utility of the libraries, we looked for differences in the expression of genes that have been broadly associated with differences in cellular proliferative activity. This comparison identified many such tags in the FL HSC library that were absent from the adult BM HSC library, including multiple cyclins (A2, B2, C, D1, D2, D3, E1, F, H, I, J L1, L2), cdc20, cdc5b, and plk, as well as 34 of the top 50 proliferation genes identified by Venezia et al (PLoS Biology, 2004) to be selectively expressed in adult BM HSCs that had been stimulated to proliferate. Other transcripts that were present at significantly higher levels in the FL HSC library (95% C.I. using Audic Claverie statistics) included msl2, rbx1, lmo2, pfn1, and 16 members of the tripartite motif protein (trim) family. Conversely, many transcripts for components of the proteosome, involved in nucleic acid binding, and transcripts coding for proteins with receptor activity were present at higher levels (or uniquely) in the adult BM HSC library. Taken together, these findings establish the validity and potential of these permanent HSC transcriptome resources for further investigation of mechanisms that determine the different biology of fetal and adult HSCs."'
GSE13264_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Liver tissue from the ""Four Core Genotype"" treated group C57BL/6J mice versus pool C57BL/6J mice of chow diet Liver"'
GSE13264_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The purpose of this experiment was to determine the expression traits in Liver tissue from the Four Core Genotype treated group. Keywords: Sry transgene Four Core Genotype Mouse liver Tissue"'
GSE13264_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Liver tissue from the ""Four Core Genotype"" treated group consists of 20 female and male C57BL/6J mice fed a chow diet containing 4% fat (Ralston-Purina Co., St. Louis, MO) until 8 weeks of age and then were gonadectomized at 8 weeks of life.  In mice of the ""four core genotypes"" (FCG), the Y chromosome is deleted for the testis-determining gene Sry, producing the Y- chromosome.  The Sry transgene is inserted onto an autosome, so that testis determination is independent of the complement of sex chromosomes.  XY-Sry gonadal males are bred with XX gonadal females, producing progeny with four different genotypes: two types of gonadal males (XX.Sry and XY-Sry) and two types of gonadal females (XX and XY-).  At 12 weeks mice were sacrificed, after a 12-hour fast, Liver tissue were dissected and flash frozen in LN2 and stored at -80°C.  All sample were compared to a common pool created from equal portions of RNA from each of the samples."'
GSE13265_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Liver tissue from hormone treated C57BL/6J mice versus pool C57BL/6J mice of chow diet Liver"'
GSE13265_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"The purpose of this experiment was to determine the expression traits in animals of inbred strain C57BL/6J, treated with gonadal hormones. (N=40, 20 males and 20 females)."'
GSE13265_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Liver tissue from the hormone treated group consists of 40 female and male C57BL/6J mice fed a chow diet containing 4% fat (Ralston-Purina Co., St. Louis, MO) until 8 weeks of age and then were gonadectomized at 8 weeks of life, implanted with hormone pellets at 12 weeks, and sacrificed at 14 weeks.  Male and female mice of the hormone treated groups received subcutaneous implants of either 0.5 mg estradiol (E2) pellet (plasma yield of 300 picogram/ml) or a 5 mg dihydrotestosterone (DHT) pellet (plasma yield of 1-2 nanogram/ml), designed to release over 21 days, (Innovative Research of America, 17B-estradiol: Cat. No. E-121 0.5mg/pellet, 5a-dihydrotestosterone: Cat. No. A-16).  Control mice were treated with the placebo pellet (Innovative Research of America, placebo: Cat. No. C-111).  At 14 weeks mice were sacrificed, after a 12-hour fast, Liver tissue were dissected and flash frozen in LN2 and stored at -80°C.  All sample were compared to a common pool created from equal portions of RNA from each of the samples. Keywords=hormone treated Mouse liver Tissue"'
GSE13277_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Specific chromatin characteristics, especially the modification status of the core histone proteins, are associated with different gene expression states. For example, active genes are marked by histone acetylation and methylation on specific lysine residues while inactive genes are marked by histones that are methylated on a different set of lysine residues and are not acetylated. There is growing interest in the chromatin characteristics of genes that respond to environmental or developmental signals with evidence that developmentally regulated genes may possess distinct chromatin marks. Using a T cell model, we examined the chromatin characteristics of inducible genes that respond to activation using ChIP-on-chip. We find that inducible genes, especially rapidly induced primary response genes, are more likely to display the chromatin characteristics of active genes, ie high levels of H3K9 acetylation. Consequently, only a small percentage of inducible genes display an increase in chromatin acetylation following activation. Our results provide evidence that inducible genes, especially rapidly induced genes, can be defined by their chromatin signature."'
GSE13277_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Specific chromatin characteristics, especially the modification status of the core histone proteins, are associated with different gene expression states. For example, active genes are marked by histone acetylation and methylation on specific lysine residues while inactive genes are marked by histones that are methylated on a different set of lysine residues and are not acetylated. There is growing interest in the chromatin characteristics of genes that respond to environmental or developmental signals with evidence that developmentally regulated genes may possess distinct chromatin marks. Using a T cell model, we examined the chromatin characteristics of inducible genes that respond to activation using ChIP-on-chip. We find that inducible genes, especially rapidly induced primary response genes, are more likely to display the chromatin characteristics of active genes, ie high levels of H3K9 acetylation. Consequently, only a small percentage of inducible genes display an increase in chromatin acetylation following activation. Our results provide evidence that inducible genes, especially rapidly induced genes, can be defined by their chromatin signature."'
GSE13277_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Cells were stimulated for 0h, 0.5h or 4h. Extracts were immunoprecipitated with either, H3K9ac, H3 or no antibody and total genomic input DNA was also collected. H3K9acetylated ChIP samples were compared to either total input genomic DNA or pan histone 3 (H3)  ChIP samples. Mock ChIP samples were compared to total input DNA. 2 biological replicates were used for all treatments except for non-stimulated EL4 cells where 3 replicates were used."'
GSE13278_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Expression microarrays were employed to identify genes induced by phorbol ester and ionomycin stimulation of EL4 cells. EL4 is a murine T cell line. To identify induced genes that were independent of new protein synthesis cells were pre-treated with cycloheximide. This expression study was used in conjunction with histone acetylation ChIP-chip to determine if inducible genes had a specific histone acetylation profile and whether the acetylation profile differed for genes with different kinetics of induction."'
GSE13278_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Expression microarrays were employed to identify genes induced by phorbol ester and ionomycin stimulation of EL4 cells. EL4 is a murine T cell line. To identify induced genes that were independent of new protein synthesis cells were pre-treated with cycloheximide. This expression study was used in conjunction with histone acetylation ChIP-chip to determine if inducible genes had a specific histone acetylation profile and whether the acetylation profile differed for genes with different kinetics of induction."'
GSE13278_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Cells were pre-treated with either DMSO or cylcoheximide in DMSO, then they were stimulated with PMA and Ionomycin for either 0h or 4h. 3 biological replicates were used for each treatment-stimulation combination."'
GSE13278_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Cells were pre-treated with either DMSO or cylcoheximide in DMSO, then they were stimulated with PMA and Ionomycin for either 0h or 4h. 3 biological replicates were used for each treatment-stimulation combination."'
GSE13281-GPL2995_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Expression profiles of  beta-hematin (BH)- or 4-hydroxy-2-nonenal (HNE)-treated RAW 264.7 cells"'
GSE13281-GPL2995_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Hemozoin phagocytosis results in immunomodulation. In the present study, gene expression profiles were analyzed to identify transcriptional changes associated with two of the individual components of Hz in a model macrophage cell line. LPS-stimulated RAW 264.7 cells were exposed to the synthetic form of Hz, β-hematin (BH, 0.1 mg/mL) and HNE (35 μM) for 6 or 24 h. "'
GSE13281-GPL2995_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Three biological replicates were analyzed for each 3 treatment types (HNE, BH, bead) in LPS stimulated cells in addition to 3 replicates of untreated LPS stimulated cells (control). Each replicate was composed of 6 pooled wells from a 6-well plate. In order to identify transcriptional changes dependent on interactions of BH rather than those due to phagocytosis, differentially expressed mRNAs were controlled by a corresponding particulate latex bead challenge."'
GSE13281-GPL6246_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Expression profiles of  beta-hematin (BH)- or 4-hydroxy-2-nonenal (HNE)-treated RAW 264.7 cells"'
GSE13281-GPL6246_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Hemozoin phagocytosis results in immunomodulation. In the present study, gene expression profiles were analyzed to identify transcriptional changes associated with two of the individual components of Hz in a model macrophage cell line. LPS-stimulated RAW 264.7 cells were exposed to the synthetic form of Hz, β-hematin (BH, 0.1 mg/mL) and HNE (35 μM) for 6 or 24 h. "'
GSE13281-GPL6246_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Three biological replicates were analyzed for each 3 treatment types (HNE, BH, bead) in LPS stimulated cells in addition to 3 replicates of untreated LPS stimulated cells (control). Each replicate was composed of 6 pooled wells from a 6-well plate. In order to identify transcriptional changes dependent on interactions of BH rather than those due to phagocytosis, differentially expressed mRNAs were controlled by a corresponding particulate latex bead challenge."'
GSE13302_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Most of the transcriptional changes induced by PFOS in the fetal mouse liver and lung were related to activation of PPARalpha.  When compared to the transcript profiles induced by PFOA (Pubmed ID 17681415), few remarkable differences were found other than up-regulation of Cyp3a genes.  Because PFOS and PFOA have been shown to differ in their mode of action in the murine neonate, these data suggest that changes related to PFOS-induced neonatal toxicity may not be evident in the fetal transcriptome at term."'
GSE13302_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Most of the transcriptional changes induced by PFOS in the fetal mouse liver and lung were related to activation of PPARalpha.  When compared to the transcript profiles induced by PFOA (Pubmed ID 17681415), few remarkable differences were found other than up-regulation of Cyp3a genes.  Because PFOS and PFOA have been shown to differ in their mode of action in the murine neonate, these data suggest that changes related to PFOS-induced neonatal toxicity may not be evident in the fetal transcriptome at term."'
GSE13305_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Molecular mechanisms underlying the metabolic changes induced by the Pro12Ala PPARγ2 variant in mice"'
GSE13306_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. This indirect effect was evident in vivo and required the expression of the RA receptor alpha. Thus, cytokine-producing CD44(hi) cells actively restrain TGF-beta-mediated Foxp3 expression in naive T cells, and this balance can be shifted or fine-tuned by RA."'
GSE13306_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. This indirect effect was evident in vivo and required the expression of the RA receptor alpha. Thus, cytokine-producing CD44(hi) cells actively restrain TGF-beta-mediated Foxp3 expression in naive T cells, and this balance can be shifted or fine-tuned by RA."'
GSE13324_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"To investigate how HOXA3 expression in wound tissue alters gene expression to control selective recruitment of bone marrow-derived cell populations, we utilized murine whole genome expression arrays (MEEBO arrays) to identify differentially expressed genes in cutaneous wounds from db/db (diabetic) mice treated with either CMV-HOXA3 or control plasmid.  In addition to unwounded control skin, we chose day 4 as the time point to harvest the wounds for RNA isolation, which represents the transition from inflammatory to proliferative phase of wound repair, and precedes the observed differences in BMDC mobilization and recruitment at day 7."'
GSE13324_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"unwounded skin, wounded skin treated with control plasmid, wounded skin treated with HOXA3"'
GSE13336_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Gene expression profiling in cardiac AngII-overexpressing mice (TG1306/1R)"'
GSE13336_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Agonist-induced cardiac hypertrophy in TG1306/1R transgenic mice with cardiac angiotensin II overproduction leads to a gradual transition from a compensatory hypertrophic state to heart failure. To gain insight into the molecular mechanisms that play a role in maintaining cardiac integrity in the diseased heart, we performed a comparative study of gene expression between wild-type (WT) and transgenic (TG) hearts using microarray analysis. TG1306/1R transgenics were separated into two phenotypic groups (hypertrophic and dilated) based on morphological parameters (cardiac weight index and histology) and either a moderate (hypertrophic) or a high (dilated) upregulation of molecular markers for hypertrophy and failure, and compared to age and sex-matched wild-types."'
GSE13364_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Microarray analysis was performed on BWF1 mice spleenocyte cells in control and pCONS treated mice."'
GSE13364_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Microarray analysis identified many genes differentially expressed in control vs pCONS treated mice spleenocytes. Some of the genes were uperegulated and some of the genes were down regulated. Microarray analysis was performed in CD4, CD8, and whole spleenocyte WBC cells."'
GSE13364_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"RNA was isolated from the mice spleenocytes from control and pCONs treated mice one week after treatment."'
GSE13380_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"The analysis includes 9 samples of genomic DNA from isolated splenic CD11c+ dendritic cells (>95% pure) per group. The two groups are neonates born to mothers with induced allergy to ovalbumin, and normal control neonates. All neonates are genetically and environmentally identical, and allergen-naive."'
GSE13382_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Allergen challenge induced mucus metaplasia modify the expression of two transcription factors belonging to the FOXA family: FOXA2 and FOXA3. Foxa2 expression is decreased during allergic airway disease whereas, Foxa3 expression is increased by allergen."'
GSE13382_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We analyzed the effects of these changes in FOXA transcription factor expression using Foxa2 transgenic mice and Foxa3-/- mice. We found that persistent expression of FOXA2 reduced mucus but the absence of FOXA3 had no effect on mucus production induced by allergen challenge."'
GSE13388_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Testosterone-induced persistent dysregulations and transdifferentiation to exocrine pancreas in the female liver"'
GSE13388_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Androgenic steroids are increasingly used for hormone therapy of postmenopausal women and abused as life style drugs and for doping purposes, though knowledge about associated health risks in females is very limited. In order to understand more about short- and long-term androgen effects on a molecular level, we have analyzed hepatic gene expression in female C57BL/6 mice immediately after subcutaneous treatment with testosterone for 3 weeks and after 12 weeks hormone withdrawal using Affymetrix array technology and quantitative real-time RT-PCR. Among about 14,000 genes examined, 48 were up- and 65 genes were downregulated by testosterone after 3-weeks treatment and about 50% of these changes persisted even 12 weeks after testostrone withdrawal.  In addition to obvious risks such as induction of hepatocellular carcinomas and virilization of liver metabolism, testosterone induced a series of changes, as e.g. dysregulation of hepatic gene expression due to incomplete conversion of female to male phenotype – in particular downregulation of cytochrom P450 isoforms and sulfotransferases. As a long-term testosterone effect, transcripts emerged in the liver that are normally specific for the exocine pancreas including amylase 2, ribonuclease 1, and several trypsin-, chymotrypsin-, and elastase-like proteases. This transdifferentiation of hepatic to exocrine pancreatic tissue indicates that testosterone can initiate long-lasting differentiation programs, which – once induced – progress even after androgen withdrawal. This may have far-reaching consequences difficult to foresee implying long-term hazards of testosterone-treatment for female health that have not been taken into account yet."'
GSE13388_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mice were treated with testosterone or sesame oil (vehicle) for three weeks twice a week. Gene expression in the liver was analyzed either directly after treatment or after three weeks of hormone/vehicle withdrawal. For each of these four groups, three individual mice were used as biological replicates."'
GSE13432_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here we show that exposure of mice to cold led to conversion of white adipose tissue (WAT) to brown-like adipose tissue, accompanying the switch of an active angiogenic phenotype.  Gene expression profile analysis showed VEGF was upregulated via most likely hypoxia-independent PGC-1 transcriptional activation.  Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis, significantly impaired nonshivering thermogenesis capacity, and markedly reduced adipose metabolism.  Unexpectedly, VEGFR1 blockage resulted in opposite effects by increasing adipose vascularity and metabolism.  These findings demonstrate that VEGFR2 and VEGFR1 mediate polarized activities in modulating adipose angiogenesis and metabolism. Taken together, our findings have conceptual implications in applying angiogenesis modulators for the treatment of obesity and metabolic disorders."'
GSE13432_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here we show that exposure of mice to cold led to conversion of white adipose tissue (WAT) to brown-like adipose tissue, accompanying the switch of an active angiogenic phenotype.  Gene expression profile analysis showed VEGF was upregulated via most likely hypoxia-independent PGC-1 transcriptional activation.  Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis, significantly impaired nonshivering thermogenesis capacity, and markedly reduced adipose metabolism.  Unexpectedly, VEGFR1 blockage resulted in opposite effects by increasing adipose vascularity and metabolism.  These findings demonstrate that VEGFR2 and VEGFR1 mediate polarized activities in modulating adipose angiogenesis and metabolism. Taken together, our findings have conceptual implications in applying angiogenesis modulators for the treatment of obesity and metabolic disorders."'
GSE13432_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here we show that exposure of mice to cold led to conversion of white adipose tissue (WAT) to brown-like adipose tissue, accompanying the switch of an active angiogenic phenotype.  Gene expression profile analysis showed VEGF was upregulated via most likely hypoxia-independent PGC-1 transcriptional activation.  Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis, significantly impaired nonshivering thermogenesis capacity, and markedly reduced adipose metabolism.  Unexpectedly, VEGFR1 blockage resulted in opposite effects by increasing adipose vascularity and metabolism.  These findings demonstrate that VEGFR2 and VEGFR1 mediate polarized activities in modulating adipose angiogenesis and metabolism. Taken together, our findings have conceptual implications in applying angiogenesis modulators for the treatment of obesity and metabolic disorders."'
GSE13443_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Mice (either C57BL/6 mice or DBA/2 mice) were randomly assigned to control group and tumor group (15 animals per group). Melanoma mice model was induced by subcutaneous (s.c.) injection of B16-F1 cells in 0.1 ml PBS into the lower-right flank of C57BL/6 mice. The lung cancer model was established by s.c. injection of KLN-205 cells in DBA/2 mice. Control animal were injected with PBS alone. Established tumors were observed after 2-3 weeks."'
GSE13443_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"When tumors reached 15 mm in diameter saliva was collected and the mice were sacrificed. Mild anesthesia was induced. Mice saliva was stimulated, obtained and immediately placed in pre-schilled 1.5-ml microcentrifuge tubes. Collection was completed in 20 minutes and samples were stored at -80ºC until analyzed.In addition, Blood was collected in BD Vacutainer tubes containing clot activator (BD Biosciences). Salivary gland and tumor tissue were removed from mice, snap-frozen in liquid nitrogen and stored at -80ºC.  "'
GSE13443_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"When tumors reached 15 mm in diameter saliva was collected and the mice were sacrificed. Mild anesthesia was induced. Mice saliva was stimulated, obtained and immediately placed in pre-schilled 1.5-ml microcentrifuge tubes. Collection was completed in 20 minutes and samples were stored at -80ºC until analyzed.In addition, Blood was collected in BD Vacutainer tubes containing clot activator (BD Biosciences). Salivary gland and tumor tissue were removed from mice, snap-frozen in liquid nitrogen and stored at -80ºC.  "'
GSE13443_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Salivary,salivary gland, serum or tumor RNA was isolated using the RNeasy Mini Kit (Qiagen) as described previously. There are 15 mice in the control group or tumor group (totally 30 C57BL/6 mice for melanoma mouse model, another 30 DBA/2 mice for lung cancer mouse model). Samples derived from 5 mice in each group were pooled and RNA extracted. The pooling is necessary to ensure sufficient salivary mRNA can be obtained for microarray analyses. Isolated total RNA was treated with recombinant DNase (Ambion, Austin, TX). For microarray analysis, mRNA from mouse saliva, gland or tumor was linearly amplified using the RiboAmp RNA Amplification kit (Molecular Devices, Sunnyvale, CA). After purification, cDNA were in vitro transcribed and biotinylated using GeneChip Expression 3’-Amplification Reagents for in vitro transcription labeling (Affymetrix, Santa Clara, CA). The labeled RNAs was subsequently fragmented, hybridization and scanning. "'
GSE13452_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Little is known about the genes involved in the initial cyst formation and disease progression in autosomal dominant polycystic kidney disease (ADPKD). To uncover the genetic determinants and molecular mechanisms of ADPKD, we analyzed 4-point time-series DNA microarrays from Pkd1L3/L3 mice to generate high-resolution gene expression profiles at different stages of disease progression. We found different characteristic gene expression signatures in the kidneys of Pkd1L3/L3 mice compared to age-matched controls during the initial phase of the disease. By postnatal week 1, the Pkd1L3/L3 kidney already had a distinctive gene expression pattern considerably different from the corresponding normal controls.  The genes differentially expressed, either induced or repressed, in ADPKD are important in immune defense, cell structure and motility, cellular proliferation, apoptosis and metabolic processes, and include members of three pathways (Wnt, Notch, and BMP) involved in morphogenetic signaling. Further analysis of the gene expression profiles from the early stage of cystogenesis to end stage disease identified a possible gene network involved in the pathogenesis of  ADPKD."'
GSE13467-GPL4128_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_overall_design	"Undifferentiated F9 cells were used for this experiment. Antibodies specificity were checked using a stable cell lines overexpressing a GAl4-Ezh1 or a Gal4-Ezh2 in an inducible manner followed by conventional ChIP at Gal4 responsive transgene. "'
GSE13467-GPL4129_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_overall_design	"Undifferentiated F9 cells were used for this experiment. Antibodies specificity were checked using a stable cell lines overexpressing a GAl4-Ezh1 or a Gal4-Ezh2 in an inducible manner followed by conventional ChIP at Gal4 responsive transgene. "'
GSE13511_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Genome-wide profiling of PPARγ:RXR and RNA polymerase II reveals temporal activation of distinct metabolic pathways in RXR dimer composition during adipogenesis."'
GSE13511_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Chromatin immunoprecipitation combined with deep sequencing was performed to generate genome-wide maps of peroxisome prolifelator-activated receptor gamma (PPARg) and retinoid X receptor (RXR) binding sites, and RNA polymerase II (RNAPII) occupancy at high resolution throughout adipocyte differentiation of 3T3-L1 cells.  The data  provides the first positional and temporal map PPARγ and RXR occupancy during adipocyte differentiation at a global scale. The number of PPARγ:RXR shared binding sites is steadily increasing from D0 to D6. At Day6 there are over 5000 high confidence shared PPARy:RXR binding sites. We show that at the early days of differentiation several of these sites bind not only PPARγ:RXR but also other RXR dimers. The data also provides a comprehensive temporal map of RNAPII occupancy at genes throughout 3T3-L1 adipogenesis thereby uncovering groups of similarly regulated genes belonging to glucose and lipid metabolic pathways. The majority of the upregulated but very few downregulated genes have assigned PPARγ:RXR target sites, thereby underscoring the importance of PPARγ:RXR in gene activation during adipogenesis and indicating that a hitherto unrecognized high number of adipocyte genes are directly activated by PPARγ:RXR"'
GSE13522_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"To investigate the early host response triggered by three different strains of Trypanosoma cruzi at a local infection site, changes in host gene expression were monitored in a murine intradermal infection model using Affymetrix oligonucleotide arrays. Robust induction of IFN-stimulated genes (ISGs) was observed in excised skin 24 hours post-infection where the level of ISG induction was parasite strain-dependent with the least virulent strain triggering a muted IFN response. Infection of mice immunodepleted of IFNγ-producing cells or infection of IFNγ-deficient mice had minimal impact on the IFN response generated in T. cruzi infected mice. In contrast, infection of mice lacking the type I IFN receptor demonstrated that type I IFNs are largely responsible for the IFN response generated at the site of infection. These data highlight type I IFNs as important components of the innate immune response to T. cruzi the site of inoculation and their role in shaping the early transcriptional response to this pathogen."'
GSE13530_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Type I interferons were discovered as the primary antiviral cytokines and are now known to serve critical functions in host defense against bacterial pathogens. Accordingly, established mediators of interferon antiviral activity may mediate previously unrecognized antibacterial functions. RNase-L is the terminal component of an RNA decay pathway that is an important mediator of interferon-induced antiviral activity. Here we identify a novel role for RNase-L in the host antibacterial response. RNase-L-/- mice exhibited a dramatic increase in mortality following "'
GSE13547_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Zfx controls BCR-induced proliferation and survival of B lymphocytes"'
GSE13547_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The development, homeostasis and function of B lymphocytes involve multiple rounds of B cell receptor (BCR)-controlled proliferation and prolonged maintenance. We analyzed the role of transcription factor Zfx, a recently identified regulator of stem cell maintenance, in B cell development and homeostasis. Conditional Zfx deletion in the bone marrow blocked B cell development at the pre-BCR selection checkpoint. Zfx deficiency in peripheral B cells caused impaired generation of the B-1 cell lineage, accelerated B cell turnover, depletion of mature recirculating cells, and delayed T-dependent antibody responses. Zfx-deficient B cells showed normal proximal BCR signaling, but impaired BCR-induced proliferation and survival. This was accompanied by aberrantly enhanced and prolonged integrated stress response, and delayed induction of Cyclin D2 and Bcl-xL proteins. Thus, Zfx restrains the stress response and couples antigen receptor signaling to B cell expansion and maintenance during development and peripheral homeostasis."'
GSE13549_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Tumor associated fibroblasts (TAF) from different tumors exhibit distinct angiogenic and tumorigenic properties. Unlike normal skin fibroblasts (NSF) or TAF (TAF-TIB6) from TIB6 tumors that are sensitive to anti-VEGF treatment, TAF (TAF-EL4) from resistant EL4 tumors can stimulate TIB6 tumor growth even when VEGF is inhibited.  We show that platelet-derived growth factor (PDGF)-C is upregulated in TAFs from resistant tumors. PDGF-C neutralizing antibodies blocked the angiogenesis induced by such TAF in vivo and slowed the growth of EL4 and admixture (TAF-EL4 + TIB6) tumors and exhibited additive effects with anti-VEGF-A antibodies. Hence, our data reveal a novel mechanism for TAF mediated tumorigenesis and suggest that some tumors may overcome inhibition of VEGF-mediated angiogenesis through upregulation of PDGF-C"'
GSE13553_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Conjugated linoleic acid (CLA), a class of fatty acids found in beef and dairy products, has been shown to inhibit tumorigenesis in a variety of cancer model systems. Based on previously well-documented anti-tumor activity of CLA in rodent models of breast cancer, a pilot study was initiated to examine the effect of dietary CLA in a well-established transgenic model of breast cancer.  Western blots were performed for the detection of AKT, c-Src, ERK1/2, and Cdc24. CLA significantly increased tumor burden (p<0.1) independent of an increase in oncogenic signaling. Mammary gland whole mounts indicated a loss of mammary adipose and extensive epithelial expansion in CLA-treated animals. Microarray analysis indicated a significant reduction in cytoskeletal related genes with at least a two-fold decrease in five out of six CLA-fed animals compared to untreated controls. Reduction of Cdc42, a key regulator of cell adhesion and cytoskeletal arrangements, was confirmed at the protein level by western blot (p<0.01). These findings suggest that dietary CLA may advance the malignant phenotype by promoting a loss of cell polarity and adhesion in the mammary gland epithelium. This action may have serious clinical implications for a subset high-risk population and warrants further investigation."'
GSE13567_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"US28-expressing and mock-transfected stable NIH-3T3 cell lines"'
GSE13582_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."'
GSE13583_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. "'
GSE13585_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."'
GSE13590_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Experimental identification of microRNA-140 targets by silencing and overexpressing miR-140"'
GSE13590_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"MicroRNAs (miRNAs) are short noncoding RNA molecules regulating the expression of mRNAs. Target identification of miRNAs is computationally difficult due to the relatively low homology between miRNAs and their targets. We present here an experimental approach to target identification where the cartilage-specific miR-140 was overexpressed and silenced in cells it is normally expressed in separate experiments. Expression of mRNAs was profiled in both experiments and the intersection of mRNAs repressed by miR-140 overexpression and derepressed by silencing of miR-140 was identified. The intersection contained only 49 genes, although both treatments affected the accumulation of hundreds of mRNAs. These 49 genes showed a very strong enrichment for the miR-140 seed sequence implying that the approach is efficient and specific. 21 of these 49 genes were predicted to be direct targets based on the presence of the seed sequence. Interestingly, none of these were predicted by the published target prediction methods we used. One of the potential target mRNAs, Cxcl12, was experimentally validated by Northern blot analysis and a luciferase reporter assay."'
GSE13592_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"CCL17-expressing dendritic cells are crucial  for the development of atherosclerosis: T cell priming"'
GSE13592_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."'
GSE13632-GPL7442_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"To test this possibility, we employed chromatin immunoprecipitation coupled to DNA microarray analysis (genome-wide location analysis or ChIP-chip) to study association of cyclin D1 with genomic DNA sequences.  In this procedure, a protein of interest is crosslinked to DNA, immunoprecipitated, and the bound DNA is hybridized to an array containing probes that span the genome.  Since anti-FLAG antibodies have been successfully used for ChIP-chip in several different systems including murine cells, knock-in mice expressing tagged cyclin D1 provided us with a novel tool to query the association of cyclin D1 with the genome in vivo, in a living mouse."'
GSE13632-GPL7443_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"To test this possibility, we employed chromatin immunoprecipitation coupled to DNA microarray analysis (genome-wide location analysis or ChIP-chip) to study association of cyclin D1 with genomic DNA sequences.  In this procedure, a protein of interest is crosslinked to DNA, immunoprecipitated, and the bound DNA is hybridized to an array containing probes that span the genome.  Since anti-FLAG antibodies have been successfully used for ChIP-chip in several different systems including murine cells, knock-in mice expressing tagged cyclin D1 provided us with a novel tool to query the association of cyclin D1 with the genome in vivo, in a living mouse."'
GSE13642_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_title	"CCL17-expressing dendritic cells are crucial  for the development of atherosclerosis"'
GSE13642_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."'
GSE13643_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"To better understand how the expression of a mutant gene that causes ALS can perturb the normal phenotype of astrocytes, and to identify genes that may have a role in their toxic effect on motor neurons, we used oligonucleotide arrays to compare the global gene expression profiles of glia overexpressing the mutant SOD1G93A protein with two different sets of controls: non-transgenic glia and glia overexpressing the wild type form of the human SOD1 protein (P<0.001) ."'
GSE13665_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"As the Crh-system and the HPA-axis are known to be crucially invovled in the onset, development and maintainance of psychiatric disorders like anxiety and depression and regulate the behavioural and endocrine stress responses the further analysis of Crhr1-dependent signaling cascades is essential to understand the molecular mechanisms behind these psychiatric diseases. In this project, new candidate genes involved in Crhr1-dependent signaling cascades were dissected using metyrapone treated stressed Crhr1-wt and -ko (Timpl et al., 1998) mice using 30 min restraint stress. Changes in mRNA expression of pituitaries of basal and stressed Crhr1-wt and -ko mice were analysed 1 and 3h, respectively, after stress begin on the Sentrix Mouse-6 Expression BeadChip."'
GSE13672-GPL1261_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_overall_design	"(corresponding to SF1, NFAT and FKHD TR families) and -224 bp(correspnding to AP2, SRF, CREB, GATA, and HOX TR families). Three other conserved motifs corresponded to ETS, EBOX, and RXR TR families. To identify TRs that potentially bind to these BEs, we carried out mRNA profiling (Affymetrix) in mouse mpkCCDc14 collecting duct cells, revealing expression of 25 TRs that are also expressed in native inner medullary collecting duct (“IMCD Transcriptome Database”). One showed a significant positive correlation with AQP2 mRNA abundance among mpkCCD subclones (Ets1) and two showed a significant negative correlation (Elf1 and an orphan nuclear receptor Nr1h2). Transcriptomic profiling in native proximal tubules (PT), medullary thick ascending limbs (MTAL) and IMCDs from kidney identified 14 TRs (including Ets1 and HoxD3) expressed in the IMCD but not PT or TAL (candidate AQP2 enhancers), and 5 TRs (including HoxA5, HoxA9 and HoxA10) expressed in PT and TAL but not in IMCD (candidate AQP2 repressors). In luciferase reporter assays, overexpression of three ETS family TRs transactivated the mouse proximal AQP2 promoter. The results implicate ETS family TRs in cell-specific expression of AQP2 and point to HOX, RXR, CREB and GATA family TRs as playing likely additional roles."'
GSE13675-GPL6845_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Cells (human and murine bone marrow mesenchymal stromal cells, and 293T cells) were treated or not with Conduritol B epoxide at 100 micromolar for 5 days, before RNA was extracted and hybridized."'
GSE13685_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Gene expression in respiratory epithelial cells treated to induce StIR"'
GSE13685_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappa-B, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."'
GSE13685_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappa-B, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."'
GSE13685_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappa-B, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."'
GSE13685_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappa-B, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."'
GSE13685_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"MLE-15 cells were treated with sham (PBS), NTHi lysate (100 ug/ml) or EF2505-III (40 ug/ml).  4 unique samples per group. Treated for 2 hours. Hybridized to Illumina Sentrix Mouse-6 v1.1 Beadhips."'
GSE13688_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"TCPOBOP (1,4-bis[2-(3,5-dichloropyridyloxy)]benzene) and PCN (pregnenolone 16α-carbonitrile) are inducers of drug metabolism through activation of nuclear receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor), respectively. Mouse experiment was designed to study the effect of CAR and PXR activation on cholesterol homeostasis genes and other genes, which are present on the Steroltalk v2 microarray. Treatments were combined with standard and high-cholesterol diet to observe the interference of high liver cholesterol on nuclear receptor transcription regulation. All experiments were done within the European sixth Framework program “Steroltalk” (www.steroltalk.net). Results form these experiments give new knowledge about involvement of ‘xenosensors’ CAR and PXR in regulation of endogenous liver metabolism."'
GSE13689_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The aim of the study was to see any effect of rosuvastatina or atorvastatin on cholesterol homeostasis after 24 hours in C57BL/6 hyperlipidemic mice (induced by diet). Experiments were perfomed using a custom Steroltalk v2 microarray. Effect of both statins on drug metabolism was also evaluated. All experiments were done within the European sixth Framework program “Steroltalk” (www.steroltalk.net)."'
GSE13691-GPL339_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Aging and neurodegeneration are often accompanied by a functionally impaired ubiquitin-proteasome system (UPS). In tauopathies and polyglutamine diseases a mutant form of Ubiquitin B, UBB+1, accumulates in disease-specific aggregates. UBB+1 mRNA is generated at low levels in vivo during transcription from the Ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB+1 accumulation, we used a UBB+1 expressing transgenic mouse line, that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimer’s disease (AD). In order to reveal affected organs and functions, young and aged UBB+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wildtype littermate mice. Accordingly, UBB+1 was strongly expressed in brainstem regions of transgenic mice controlling respiration. These regions included, for example, the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nuclei. In addition, UBB+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented controls. We conclude that long-term UPS inhibition due to UBB+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients."'
GSE13691-GPL340_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Aging and neurodegeneration are often accompanied by a functionally impaired ubiquitin-proteasome system (UPS). In tauopathies and polyglutamine diseases a mutant form of Ubiquitin B, UBB+1, accumulates in disease-specific aggregates. UBB+1 mRNA is generated at low levels in vivo during transcription from the Ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB+1 accumulation, we used a UBB+1 expressing transgenic mouse line, that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimer’s disease (AD). In order to reveal affected organs and functions, young and aged UBB+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wildtype littermate mice. Accordingly, UBB+1 was strongly expressed in brainstem regions of transgenic mice controlling respiration. These regions included, for example, the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nuclei. In addition, UBB+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented controls. We conclude that long-term UPS inhibition due to UBB+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients."'
GSE13705-GPL339_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"The effects of dietary curcumin on colonic gene expression in TNBS-induced colitis"'
GSE13705-GPL339_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Curcumin is a potent anti-inflammatory compound capable of preventing chemically induced colitis in mice."'
GSE13705-GPL339_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We used microarray analysis to detail the global programme of colonic gene expression in BALB/c mice fed standard or 2% curcumin-supplemented diet and treated with control or TNBS (trnitrobenzene-sulfonic acid, 2 mg/mouse) enema."'
GSE13705-GPL339_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"6-8 week old BALB/c mice were treated with respecive diet two days prior to enema administration (day 0) and sacrificed on day 7. Whole colon was dissected from  mice and their wild-type littermates and total RNA isolated for microarray analysis using Affymetrix murine MOE430 mouse array set. RNA was pooled from 3 mice in each dietary/treatment group."'
GSE13705-GPL340_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"The effects of dietary curcumin on colonic gene expression in TNBS-induced colitis"'
GSE13705-GPL340_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Curcumin is a potent anti-inflammatory compound capable of preventing chemically induced colitis in mice."'
GSE13705-GPL340_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We used microarray analysis to detail the global programme of colonic gene expression in BALB/c mice fed standard or 2% curcumin-supplemented diet and treated with control or TNBS (trnitrobenzene-sulfonic acid, 2 mg/mouse) enema."'
GSE13705-GPL340_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"6-8 week old BALB/c mice were treated with respecive diet two days prior to enema administration (day 0) and sacrificed on day 7. Whole colon was dissected from  mice and their wild-type littermates and total RNA isolated for microarray analysis using Affymetrix murine MOE430 mouse array set. RNA was pooled from 3 mice in each dietary/treatment group."'
GSE13707_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Keywords: Differential expression in treated and control mice"'
GSE13707_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Ten samples from JA16 antibody-treated mice were compared with 10 samples from saline-treated mice"'
GSE13718_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Results: Ebp1 -/- mice were on average 30% smaller than wild type and heterozygous sex matched littermates. Growth retardation was apparent from Day 10 until Day 30. IGF-1 production and IGBP-3 and 4 protein levels were reduced in  both embryo fibroblasts and adult knock-out mice. The proliferation of fibroblasts derived from Day 12.5  knock out embryos was also decreased as compared to that of wild type cells. Microarray expression analysis revealed changes in genes important in cell growth including members of the MAPK signal transduction pathway. In addition, the expression or activation of proliferation related genes such as AKT and the androgen receptor, previously demonstrated to be affected by Ebp1 expression in vitro,  were altered in adult tissues."'
GSE13719_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"TCDD induced gene expression changes in dendritic cells"'
GSE13719_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Effect of the over activation of the aryl hydrocarbon receptor on gene expression of spleen derived dendritic cells. "'
GSE13730_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"BALB/c mice genetically susceptible to proteoglycan-induced arthritis and spondylitis"'
GSE13730_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), a murine model of rheumatoid arthritis (Glant,T.T. and Mikecz,K., Proteoglycan aggrecan-induced arthritis.  A murine autoimmune model of rheumatoid arthritis. Methods Mol.Med. 2004. 102: 313-338.). However, there are marked differences among BALB/c colonies (maintained by different vendors at different locations) in PGIA onset and severity, which could be the result of subtle variations in their genetic background."'
GSE13740_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_title	"Gene expression in C57BL/6 mouse lungs after exposure to aerosolized NTHi lysate"'
GSE13740_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappaB, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."'
GSE13740_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappaB, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."'
GSE13740_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappaB, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."'
GSE13740_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappaB, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."'
GSE13740_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"Gene expression patterns in mouse lung homogenates were analyzed 2h after exposure to aerosolized PBS (Sham treatment), 2h after exposure to aerosolized NTHi lysate or 4h after exposure to aerosolized NTHi lysate.  Each group consisted of six mice."'
GSE13770_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The concept of dedifferentiation of somatic cells into pluripotent stem cells has opened a new era in regenerative medicine. Viral transduction of defined factors has successfully achieved pluripotency derived from somatic cells. However, during the generation process of induced pluripotent stem (iPS) cells, genetic integration of certain factors may cause mutagenesis or tumorigenicity, which limits further application. Therefore, there is currently ongoing an extensive search for new methods such as transient gene delivery and oocyte-free and non-viral inducers like small molecules. Here we show that the transient delivery of embryonic stem (ES) cell-derived soluble proteins enables dedifferentiation of mouse adult somatic cells converting them into pluripotent stem cells without the introduction of certain transcription factors or genetic manipulation. During the dedifferentiation, global gene expression patterns and epigenetic status were converted from the somatic to the ES-equivalent status. Dedifferentiated somatic cells were morphologically, biologically and functionally indistinguishable from ES cells. Furthermore, the dedifferentiated cells possessed in vivo differentiation and development potential. Our results provide an alternative and safe strategy for dedifferentiation of somatic cells that can be used to facilitate pluripotent stem cell-based cell therapy."'
GSE13772_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"The apoA-I induced transcriptome and dependence on MyD88"'
GSE13772_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Apolipoprotein A-I is well known to play a role in cholesterol efflux, but our studies suggest that apoA-I may also induce proinflammatory signaling.  The molecular mechanisms behind apoA-I-mediated proinflammatory signaling have not yet been explored, nor has the link between this signaling and cholesterol efflux. We hypothesize that apoA-I is a novel TLR agonist, signaling through the MyD88 proinflammatory signaling adaptor to induce cytokines.  Microarray analysis confirmed that a suite of pro-inflammatory genes are induced by apoA-I with varying dependence upon MyD88, and that MyD88 regulates >6% of the apoA-I-induced transcriptome."'
GSE13772_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Three replicate experiments were analyzed.  Each experiment consisted of a control sample and an apoA-I treated sample of RNA extracted from peritoneal macrophages isolated from both MyD88 +/+ and MyD88-/- mice, totaling four samples per experiment; 12 samples together."'
GSE13782_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Identification of spondylarthropathy-specific genes in BALB/c mice with proteoglycan-induced spondylitis (PGIS)"'
GSE13795_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Cardiac function is regulated by many hormones and neurotransmitters which exert their physiological effects through the activation of G protein-coupled receptors (GPCRs). Here, we quantified the expression of 395 endoGPCRs (all GPCRs excluding taste and odorant receptors) in male mouse right and left atria and ventricles by using high-throughput real-time RT-PCR and focused on the 135 most highly expressed transcripts. No cardiac functional data is available for almost half of these receptors. Cluster analysis allowed us to link GPCR expression patterns to cardiac function. Indeed, ventricles and atria are both contractile; however, the latter, and especially the right atrium, are central to the generation and regulation of cardiac rhythm. Accordingly, the right atrium exhibited the most specific signature whereas the vast majority of GPCRs found in ventricles were evenly expressed in both the right and left chambers. RT-PCR data were confirmed at the protein level for six selected transcripts (ETA, EP1, PAR1, Sfrp1, CCR2 and AT1a) and at the functional level in isolated mouse ventricular cardiomyocytes for the glutamate metabotropic receptor 1b."'
GSE13823-GPL339_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The aim of this work was to determine the genes and mechanisms involved in IL-9- and CCL1-mediated protection against glucocorticoid-induced apoptosis. We made the hypothesis that the expression of the really critical mediators could be regulated in a reciprocal way by Dex on the one hand and anti-apoptotic cytokines such as IL-9 and CCL1 on the other hand.Therefore, we performed a comprehensive study of the genes expressed by BW5147 cells stimulated with or without Dex, IL-9 and CCL1, taking advantage of the Affymetrix microarray technology."'
GSE13823-GPL339_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"The aim of this work was to determine the genes and mechanisms involved in IL-9- and CCL1-mediated protection against glucocorticoid-induced apoptosis. We made the hypothesis that the expression of the really critical mediators could be regulated in a reciprocal way by Dex on the one hand and anti-apoptotic cytokines such as IL-9 and CCL1 on the other hand.Therefore, we performed a comprehensive study of the genes expressed by BW5147 cells stimulated with or without Dex, IL-9 and CCL1, taking advantage of the Affymetrix microarray technology."'
GSE13823-GPL339_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"One million BW5147 cells were stimulated with 100 ng/ml of dexamethasone and/or with 100 U/ml of IL-9 or CCL1 for eight hours. RNA was then extracted for  hybridization on Affymetrix microarrays. This experiment was performed in duplicates ."'
GSE13823-GPL8321_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The aim of this work was to determine the genes and mechanisms involved in IL-9- and CCL1-mediated protection against glucocorticoid-induced apoptosis. We made the hypothesis that the expression of the really critical mediators could be regulated in a reciprocal way by Dex on the one hand and anti-apoptotic cytokines such as IL-9 and CCL1 on the other hand.Therefore, we performed a comprehensive study of the genes expressed by BW5147 cells stimulated with or without Dex, IL-9 and CCL1, taking advantage of the Affymetrix microarray technology."'
GSE13823-GPL8321_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"The aim of this work was to determine the genes and mechanisms involved in IL-9- and CCL1-mediated protection against glucocorticoid-induced apoptosis. We made the hypothesis that the expression of the really critical mediators could be regulated in a reciprocal way by Dex on the one hand and anti-apoptotic cytokines such as IL-9 and CCL1 on the other hand.Therefore, we performed a comprehensive study of the genes expressed by BW5147 cells stimulated with or without Dex, IL-9 and CCL1, taking advantage of the Affymetrix microarray technology."'
GSE13823-GPL8321_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"One million BW5147 cells were stimulated with 100 ng/ml of dexamethasone and/or with 100 U/ml of IL-9 or CCL1 for eight hours. RNA was then extracted for  hybridization on Affymetrix microarrays. This experiment was performed in duplicates ."'
GSE13840_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Despite years of effort, exact pathogenesis of non-alcoholic fatty liver disease (NAFLD) remains obscure. To gain an insight into the regulatory roles of microRNAs (miRNAs) in aberrant energy metabolic status and pathogenesis of NAFLD, we analyzed the expression of miRNAs in livers of ob/ob mice, streptozotocin (STZ)-induced type 1 diabetic mice and normal C57BL/6 mice by miRNA microarray. Compared to normal C57BL/6 mice, ob/ob mice showed up-regulation of 8 miRNAs and down-regulation of 4 miRNAs in fatty livers. Up-regulation of miR-34a and down-regulation of miR-122 was found in livers of STZ-induced diabetic mice. These results demonstrate that distinct miRNAs are strongly dysregulated in NAFLD and hyperglycemia. Comparison between miRNA expressions in livers of ob/ob mice and STZ-administered mice further revealed up-regulation of 4 miRNAs and down-regulation of 2 miRNAs in livers of ob/ob mice, indicating that these miRNAs may represent a molecular signature of NAFLD. A distinctive miRNA expression pattern was identified in ob/ob mouse liver and hierarchical clustering of this pattern could clearly discriminate ob/ob mice from either normal C57BL/6 mice or STZ-administered mice. These findings suggest an important role of miRNAs in hepatic energy metabolism and implicate the participation of miRNAs in the pathophysiological processes of NAFLD."'
GSE13840_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"In the present study, we analyzed the expression of miRNAs in livers of 10 ob/ob mice, 8 streptozotocin (STZ)-induced type 1 diabetic mice and 8 normal control C57BL/6 mice by miRNA microarray."'
GSE13858-GPL5105_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"To examine the effect of E2 treatment for the miRNA expression, at 15 week old, female wiled type mice were ovariectomized, and after one week, estradiol (E2) was delivered at a concentration of 0.050 mg/kg body weight/day. 24 hours after chemical treatment, uteruses from mice treated with or without E2 were dissected. "'
GSE13858-GPL5106_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"To examine the effect of E2 treatment for the miRNA expression, at 15 week old, female wiled type mice were ovariectomized, and after one week, estradiol (E2) was delivered at a concentration of 0.050 mg/kg body weight/day. 24 hours after chemical treatment, uteruses from mice treated with or without E2 were dissected. "'
GSE13873_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Chronic infection with the bacterial pathogen Helicobacter pylori is a risk factor for the development of gastric cancer, yet remains asymptomatic in a majority of individuals. We report here that the C57Bl6 mouse model of experimental infection with the closely related H. felis recapitulates this wide range in host susceptibility. A majority of infected mice develop premalignant lesions such as gastric atrophy, compensatory epithelial hyperplasia and intestinal metaplasia, whereas a minority is completely protected from preneoplasia. Protection is associated with the failure to mount an IFN-gamma response to the infection and an associated high Helicobacter burden. We demonstrate that IFN-gamma is essential for clearance of Helicobacter, but also mediates the formation of preneoplastic lesions. We further provide evidence that IFN-gamma triggers a specific transcriptional program in murine gastric epithelial cells in vitro and in vivo, and induces their preferential transformation to the hyperplastic phenotype. In summary, our data suggest a dual role for IFN-gamma in Helicobacter pathogenesis that could provide an explanation for the differential susceptibility to H. pylori-induced gastric pathology in the human population."'
GSE13873_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"We chose mice for gene expression profiling that following Helicobacter infection had (a) symptoms of gastritis, but no epithelial changes, (b) atrophic gastritis accompanied by corpus gland hyperplasia or (c) atrophic gastritis accompanied by intestinal metaplasia. An uninfected control group was also included in the analysis, as were two groups of mice that lacked mature T- and B-cells due to a deletion mutation in the rag1 gene (Rag-1-/-) and that were either experimentally infected or served as Rag-1-/- uninfected controls. To see the effects of IFNg on murine gastric epithelial cells we analysed an immortalized murine primary gastric epithelial cell line treated with three different concentrations of IFNg in comparison to an untreated control."'
GSE13874-GPL1261_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"We show that miR-1 is downregulated in a murine heart failure model. miRNAs expression changes were measured in calcineurin transgenic model of heart failure and control mice using a Luminex platform. Reduced miR-1 expression was associated with broad alteration in expression of predicted target genes. To test this, we measured miRs including miR-1 and genome wide transcriptome changes in vivo and in vitro system. Calcineurin transgenic heart was compared to nontransgenic heart (NTg vs. CNTg). We also investigated the gene expression changes during the course of cardiomyocytes differentiation using DMSO treated P19CL6 cell lines. Two time points (day 6 and day 10) were compared to identified the gene expression changes of predicted miR-1 targets (Day 6 vs. Day 10). "'
GSE13874-GPL8225_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"We show that miR-1 is downregulated in a murine heart failure model. miRNAs expression changes were measured in calcineurin transgenic model of heart failure and control mice using a Luminex platform. Reduced miR-1 expression was associated with broad alteration in expression of predicted target genes. To test this, we measured miRs including miR-1 and genome wide transcriptome changes in vivo and in vitro system. Calcineurin transgenic heart was compared to nontransgenic heart (NTg vs. CNTg). We also investigated the gene expression changes during the course of cardiomyocytes differentiation using DMSO treated P19CL6 cell lines. Two time points (day 6 and day 10) were compared to identified the gene expression changes of predicted miR-1 targets (Day 6 vs. Day 10). "'
GSE13916_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Overexpression and/or amplification of the ErbB-2 oncogene, as well as inactivation of the tumor suppressor PTEN, are two important genetic events in human breast carcinogenesis.  To address the biological impact of conditional inactivation of PTEN on ErbB-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the MMTV promoter to directly couple expression of activated ErbB-2 and Cre recombinase to the same mammary epithelial cell (MMTV-NIC).  Disruption of PTEN in the mammary epithelium of the MMTV-NIC model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  PTEN-deficient/NIC tumorigenesis was associated with an increase in angiogenesis. Moreover, inactivation of PTEN in the MMTV-NIC mouse model resulted in hyperactivation of the PI3K/Akt signalling pathway. However, like the parental strain, tumors obtained from PTEN-deficient/NIC mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  Taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by PTEN deficiency and ErbB-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."'
GSE13916_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Overexpression and/or amplification of the ErbB-2 oncogene, as well as inactivation of the tumor suppressor PTEN, are two important genetic events in human breast carcinogenesis.  To address the biological impact of conditional inactivation of PTEN on ErbB-2-induced mammary tumorigenesis, we generated a novel transgenic mouse model that utilizes the MMTV promoter to directly couple expression of activated ErbB-2 and Cre recombinase to the same mammary epithelial cell (MMTV-NIC).  Disruption of PTEN in the mammary epithelium of the MMTV-NIC model system dramatically accelerated the formation of multifocal and highly metastatic mammary tumors, which exhibit homogenous pathology.  PTEN-deficient/NIC tumorigenesis was associated with an increase in angiogenesis. Moreover, inactivation of PTEN in the MMTV-NIC mouse model resulted in hyperactivation of the PI3K/Akt signalling pathway. However, like the parental strain, tumors obtained from PTEN-deficient/NIC mice displayed histopathological and molecular features of the luminal-like subtype of breast cancer.  Taken together, our findings provide important implications in understanding the molecular determinants of mammary tumorigenesis driven by PTEN deficiency and ErbB-2 activation, and could provide a valuable tool for testing the efficacy of therapeutic strategies that target these critical signalling pathways."'
GSE13946_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Comparison of gamma delta intraepithelial lymphocytes from DSS-treated and untreated colon"'
GSE13946_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"gamma delta intraepithelial lymphocytes were isolated from the colons of DSS-treated and untreated mice. Total RNAs were isolated and compared by Affymetrix DNA microarray."'
GSE13946_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Duplicate comparisons were made between DSS-treated and untreated gamma delta intraepithelial lymphocytes."'
GSE13948_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"MicroRNA-122 (miR-122) is an abundant liver-specific miRNA, implicated in fatty acid and cholesterol metabolism as well as hepatitis C viral replication. Here, we report that a systemically administered 16-nt, unconjugated LNA (locked nucleic acid)-antimiR oligonucleotide complementary to the 5' end of miR-122 leads to specific, dose-dependent silencing of miR-122 and shows no hepatotoxicity in mice. Antagonism of miR-122 is due to formation of stable heteroduplexes between the LNA-antimiR and miR-122 as detected by northern analysis. Fluorescence in situ hybridization demonstrated uptake of the LNA-antimiR in mouse liver cells, which was accompanied by markedly reduced hybridization signals for mature miR-122 in treated mice. Functional antagonism of miR-122 was inferred from a low cholesterol phenotype and de-repression within 24 h of 199 liver mRNAs showing significant enrichment for miR-122 seed matches in their 3' UTRs. Expression profiling extended to 3 weeks after the last LNA-antimiR dose revealed that most of the changes in liver gene expression were normalized to saline control levels coinciding with normalized miR-122 and plasma cholesterol levels. Combined, these data suggest that miRNA antagonists comprised of LNA are valuable tools for identifying miRNA targets in vivo and for studying the biological role of miRNAs and miRNA-associated gene-regulatory networks in a physiological context."'
GSE13948_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Female NMRI mice were treated at day 2 with either 25mg/kg antimiR-122 (SPC3372) or vehicle (saline). Mice were sacrificied at day 3, 9 and 23 and liver RNA assayed. Three biological replicates for each of the six groups."'
GSE13963_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Molecular characterization of lung dysplasia induced by c-raf-1"'
GSE13974_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Abnormal N-methyl-D-aspartate receptor (NMDAR) function has been implicated in the pathophysiology of schizophrenia.  D-serine is an important NMDAR modulator, and to elucidate the role of the D-serine synthesis enzyme serine racemase (Srr) in schizophrenia, we identified and characterized mice with an ENU-induced mutation that results in a complete loss of Srr activity and drastically reduced D-serine levels.  Mutant mice displayed behaviors relevant to schizophrenia, including impairments in prepulse inhibition, sociability and spatial discrimination.  Behavioral deficits were rescued by D-serine and the atypical antipsychotic clozapine, and were conversely, amplified by NMDAR inhibition.  Expression profiling revealed that the Srr mutation influenced several genes that have been linked to schizophrenia and cognitive ability.  Furthermore, analysis of Srr genetic variants in humans identified a robust association with schizophrenia.  This study demonstrates that aberrant serine racemase function and diminished D-serine may contribute to schizophrenia pathogenesis, and that D-serine may be a beneficial form of treatment"'
GSE13979_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"We have investigated the regulation of anchorage-independent growth (AIG) by basic fibroblast growth factor (bFGF) and 12-O-tetradecanoyl phorbol-13-acetate (TPA) in JB6 mouse epidermal cells in the context of wound repair versus carcinogenesis responses.  bFGF induces an unusually efficient but reversible AIG response, relative to TPA-induced AIG which is irreversible.  Distinct global gene expression profiles are associated with anchorage-independent colonies arising from bFGF-stimulated JB6 cells, relative to colonies arising from fully tumorigenic JB6 cells (RT101), including genes exhibiting reciprocal regulation patterns.  Thus, while TPA exposure results in commitment to an irreversible and tumorigenic AIG phenotype, the AIG response to bFGF is reversible with essentially complete restoration of normal cell cycle check point control following removal of bFGF from growth medium.  These results are consistent with the physiological role of bFGF in promoting wound healing, and suggest that natural mechanisms exist to reverse transformative cellular phenotypes associated with carcinogenesis."'
GSE13979_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We have investigated the regulation of anchorage-independent growth (AIG) by basic fibroblast growth factor (bFGF) and 12-O-tetradecanoyl phorbol-13-acetate (TPA) in JB6 mouse epidermal cells in the context of wound repair versus carcinogenesis responses.  bFGF induces an unusually efficient but reversible AIG response, relative to TPA-induced AIG which is irreversible.  Distinct global gene expression profiles are associated with anchorage-independent colonies arising from bFGF-stimulated JB6 cells, relative to colonies arising from fully tumorigenic JB6 cells (RT101), including genes exhibiting reciprocal regulation patterns.  Thus, while TPA exposure results in commitment to an irreversible and tumorigenic AIG phenotype, the AIG response to bFGF is reversible with essentially complete restoration of normal cell cycle check point control following removal of bFGF from growth medium.  These results are consistent with the physiological role of bFGF in promoting wound healing, and suggest that natural mechanisms exist to reverse transformative cellular phenotypes associated with carcinogenesis."'
GSE13979_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"We have investigated the regulation of anchorage-independent growth (AIG) by basic fibroblast growth factor (bFGF) and 12-O-tetradecanoyl phorbol-13-acetate (TPA) in JB6 mouse epidermal cells in the context of wound repair versus carcinogenesis responses.  bFGF induces an unusually efficient but reversible AIG response, relative to TPA-induced AIG which is irreversible.  Distinct global gene expression profiles are associated with anchorage-independent colonies arising from bFGF-stimulated JB6 cells, relative to colonies arising from fully tumorigenic JB6 cells (RT101), including genes exhibiting reciprocal regulation patterns.  Thus, while TPA exposure results in commitment to an irreversible and tumorigenic AIG phenotype, the AIG response to bFGF is reversible with essentially complete restoration of normal cell cycle check point control following removal of bFGF from growth medium.  These results are consistent with the physiological role of bFGF in promoting wound healing, and suggest that natural mechanisms exist to reverse transformative cellular phenotypes associated with carcinogenesis."'
GSE13979_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"To determine whether there were shared transcriptional effects between reversible and irreversible AIG, we performed global microarray analyses on colonies isolated from soft agar for both bFGF-treated JB6 cells and fully tumorigenic JB6 cells from the RT101 cell line.  Gene expression changes associated with colony formation were determined by comparison to respective monolayer control cells."'
GSE13986_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"MTB/TRAS short-term induction, tumor, and TGFbeta treated NMuMG cells"'
GSE13986_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"To test whether SVD regression is sufficiently sensitive to detect activation of a secondary, endogenous pathway as it occurs following ectopic manipulation of a strong primary pathway by focusing on the relationship between the Ras and TGFβ signaling pathways."'
GSE13992_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"For gene array analysis c-MetDhepa and c-MetloxP/loxP controls were stimulated for 2 hours with 2µg recombinant mouse HGF.Three animals per group were treated in parallel, before and after i.p. injection of recombinant HGF or NaCl."'
GSE13992_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"For gene array analysis c-MetDhepa and c-MetloxP/loxP controls were stimulated for 2 hours with 2µg recombinant mouse HGF.Three animals per group were treated in parallel, before and after i.p. injection of recombinant HGF or NaCl."'
GSE14004_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"This dataset consists of three sample groups: preadipocytes, control siRNA treated adipocytes, and PPAR gamma siRNA treated adipocytes.  Each sample group consists of three replicates samples.  Each sample was hybridized to a separate array for a total of nine arrays."'
GSE14012-GPL1261_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Induced pluripotent stem (iPS) cells can be obtained from fibroblasts by expression of Oct4, Sox2, Klf4, and c-Myc. To determine how these factors induce this change in cell identity, we carried out genomewide promoter analysis of their binding in iPS and partially reprogrammed cells. Most targets in iPS cells are shared with ES cells and the factors cooperate to activate the ES-like expression program. In partially reprogrammed cells, genes bound by c-Myc have achieved a more ES-like binding and expression pattern. In contrast, genes that are co-bound by Oct4, Sox2, and Klf4 in ES cells and that encode pluripotency regulators show severe lack of both binding and transcriptional activation. Among the factors, c-Myc has a pivotal effect on the initiation of the ES transcription program, including the repression of fibroblast-specific genes. Our analysis begins to unravel how the four factors function together and suggests a temporal and separable order of their effects during reprogramming."'
GSE14012-GPL7777_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Induced pluripotent stem (iPS) cells can be obtained from fibroblasts by expression of Oct4, Sox2, Klf4, and c-Myc. To determine how these factors induce this change in cell identity, we carried out genomewide promoter analysis of their binding in iPS and partially reprogrammed cells. Most targets in iPS cells are shared with ES cells and the factors cooperate to activate the ES-like expression program. In partially reprogrammed cells, genes bound by c-Myc have achieved a more ES-like binding and expression pattern. In contrast, genes that are co-bound by Oct4, Sox2, and Klf4 in ES cells and that encode pluripotency regulators show severe lack of both binding and transcriptional activation. Among the factors, c-Myc has a pivotal effect on the initiation of the ES transcription program, including the repression of fibroblast-specific genes. Our analysis begins to unravel how the four factors function together and suggests a temporal and separable order of their effects during reprogramming."'
GSE14021_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"The molecular mechanisms that lead to the cognitive defects characteristic of Down syndrome (DS), the most frequent cause of mental retardation, have remained elusive. Here we use a transgenic DS mouse model to show that DYRK1A gene dosage imbalance deregulates chromosomal clusters of genes located near neuron-restrictive silencer factor (REST/NRSF) binding sites. We found that DYRK1A binds the SWI/SNF-complex known to interact with REST/NRSF. Mutation of a REST/NRSF binding site in the promoter of the REST/NRSF target gene L1cam modifies the transcriptional effect of Dyrk1A-dosage imbalance on L1cam. DyrkA dosage imbalance perturbs Rest/Nrsf levels with decreased Rest/Nrsf expression in embryonic neurons and increased expression in adult neurons. We identified a coordinated deregulation of multiple genes that are responsible for the cellular phenotypic traits present in DS such as dendritic growth impairment and microcephaly during prenatal cortex development. Dyrk1a overexpression in primary mouse cortical neurons reduced the neuritic complexity. In the postnatal hippocampus, DYRK1A overexpression suppresses a form of synaptic plasticity that may be sufficient to cause DS cognitive defects. We propose that DYRK1A overexpression-related neuronal gene deregulation generates the brain phenotypic changes that characterize DS, with an accessory role for the gene dosage imbalance of other chromosome 21 genes."'
GSE14024_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The insulin-like growth factor (IGF) axis is an important signaling pathway in the growth and survival of many cell types and has been implicated in multiple aspects of cancer progression from tumorigenesis to metastasis. The multiple roles of IGF signaling in cancer suggest that selective inhibition of the pathway might yield clinically effective therapeutics. Here we describe A-928605, a novel small molecule inhibitor of the receptor tyrosine kinase responsible for IGF signal transduction. This small molecule is able to abrogate activation of the pathway as shown by effects on the target and downstream effectors and is shown to be effective at inhibiting the proliferation of an oncogene addicted tumor model cell line (CD8-IGF1R 3T3) both in vitro and in vivo. "'
GSE14024_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"CD8-IGF1R 3T3 cells and 3T3 Vector control treated for 24 h with vehicle or IGF1R inhibitor A-928605, all with 3 replicates."'
GSE14030_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"The molecular mechanisms that lead to the cognitive defects characteristic of Down syndrome (DS), the most frequent cause of mental retardation, have remained elusive. Here we use a transgenic DS mouse model to show that DYRK1A gene dosage imbalance deregulates chromosomal clusters of genes located near neuron-restrictive silencer factor (REST/NRSF) binding sites. We found that DYRK1A binds the SWI/SNF-complex known to interact with REST/NRSF. Mutation of a REST/NRSF binding site in the promoter of the REST/NRSF target gene L1cam modifies the transcriptional effect of Dyrk1A-dosage imbalance on L1cam. DyrkA dosage imbalance perturbs Rest/Nrsf levels with decreased Rest/Nrsf expression in embryonic neurons and increased expression in adult neurons. We identified a coordinated deregulation of multiple genes that are responsible for the cellular phenotypic traits present in DS such as dendritic growth impairment and microcephaly during prenatal cortex development. Dyrk1a overexpression in primary mouse cortical neurons reduced the neuritic complexity. In the postnatal hippocampus, DYRK1A overexpression suppresses a form of synaptic plasticity that may be sufficient to cause DS cognitive defects. We propose that DYRK1A overexpression-related neuronal gene deregulation generates the brain phenotypic changes that characterize DS, with an accessory role for the gene dosage imbalance of other chromosome 21 genes."'
GSE14030_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_overall_design	"Agilent Whole Mouse Genome oligomicroarrays (GEO accession no. GPL2872, Agilent Technologies, Palo Alto, CA) were used. They contain 60-mer DNA probes synthesized in situ in a 44k format. Of 44,290 spots, 2756 are controls. The remaining 41,534 spots represent 33,661 unique transcripts which correspond to 20,202 unique human genes. Five independent (Dyrk1A overexpression, five individual samples) measurements were carried out for each group of biological conditions using exchanged dye-labeled RNA targets (i.e., Cy3 and Cy5 dye-swapping experiments). "'
GSE14035_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Diabetes mellitus [DM], with its burden of premature morbidity and mortality, represents one of the major threats to human health in the 21st century (Zimmet 2001). Accelerated atherosclerosis affecting arteries that supply the heart, brain and lower extremities is responsible for an increased risk of acute ischemic events. DM is also associated with microvascular disease, which is a leading cause of blindness, renal failure and debilitating neuropathies. Endothelial dysfunction, increased vascular permeability and microvascular cell loss by apoptosis are all hallmarks of diabetic microangiopathy. Diabetic patients not only incur cardiovascular complications more frequently, but also experience worse outcomes due to attenuation of vascular repair mechanisms. This impairment includes quantitative and qualitative abnormalities of bone marrow [BM]-derived progenitor cells (Emanueli 2002&2004; Loomans 2004; Krankel 2005; Fadini 2006). The mechanisms underlying BM dysfunction remain however enigmatic, especially when considering the privileged location that protects stem cells [SC] and progenitor cells [PC] of the marrow from external insults (Kopp 2008 and Kiel 2008). BM endothelial cells [EC] are instead an obvious target of DM, because they are directly exposed to blood glucose and incapable to regulate glucose influx. Strangely enough, little is known about the impact of diabetes on BM microvasculature. We hypothesize that damage induced by DM might start at the microvascular level, in a similar fashion to microangiopathy, which occurs in kidney, retina, heart and brain. We also propose that enduring microvascular cell loss might result in marrow hypo-perfusion and destabilization of SC homeostasis."'
GSE14035_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"In order to test this hypothesis, we studied streptozotocin-induced (STZ) type-1 DM and age-matched non-DM mice (n=6 to 10 per group in each experiment). Histological examination of femurs, collected from STZ-mice at 28-30 weeks from induction of DM or controls, showed remarkable differences in bone density and marrow composition. Bone marrow cells from healthy and diabetic animals were next selected for endothelial progenitors and cultured for 10 days under endothelial cell growth conditions. Next RNA was isolated and analysed by Illumina Sentrix Beadarrays."'
GSE14071_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The inflammatory response plays out over time in a reproducible and organized manner after an initiating stimulus. Here we showed that the genes activated in cultured mouse fibroblasts in response to the proinflammatory cytokine tumor necrosis factor can be divided roughly into three groups, each with different induction kinetics. Whereas differential transcription is important in determining the grouping of these genes, differential mRNA stability also exerted strong influence in some cases overriding that of transcriptional control elements on the temporal order of gene expression. mRNA transcripts expressed early after TNF stimulation have abundant AU-rich elements in their 3'-untranslated regions whereas those expressed later are contain fewer AU-rich sequences. Thus mRNA stability and transcriptional control, two intrinsic characteristics of genes, control the kinetics of proinflammatory cytokine-induced gene expression."'
GSE14071_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"The gene expression levels were monitored in the mouse embryonic cells stimulated with TNF for 0, 0.5h, 2h and 12 hours."'
GSE14072_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"REST/NRSF target gene L1cam modifies the transcriptional effect of Dyrk1Adosage imbalance on L1cam. DyrkA dosage imbalance perturbs Rest/Nrsf levels with decreased Rest/Nrsf expression in embryonic neurons and increased expression in adult neurons. We identified a coordinated deregulation of multiple genes that are responsible for the cellular phenotypic traits present in DS such as dendritic growth impairment and microcephaly during prenatal cortex development. Dyrk1a overexpression in primary mouse cortical neurons reduced the neuritic complexity. In the postnatal hippocampus, DYRK1A overexpression suppresses a form of synaptic plasticity that may be sufficient to cause DS cognitive defects. We propose that DYRK1A overexpression-related neuronal gene deregulation generates the"'
GSE14088_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Ubiquitin and ubiquitin-like proteins (UBLs) are directed to targets by cascades of E1, E2, and E3 enzymes. The largest ubiquitin E3 subclass consists of cullin-RING ligases (CRLs), which contain one each of several cullins (CUL1, -2, -3, -4, or -5) and RING proteins (RBX1 or -2). CRLs are activated by ligation of the UBL NEDD8 to a conserved cullin lysine. How is cullin NEDD8ylation specificity established? Here we report that, like UBE2M (also known as UBC12), the previously uncharacterized E2 UBE2F is a NEDD8-conjugating enzyme in vitro and in vivo. Biochemical and structural analyses indicate how plasticity of hydrophobic E1-E2 interactions and E1 conformational flexibility allow one E1 to charge multiple E2s. The E2s have distinct functions, with UBE2M/RBX1 and UBE2F/RBX2 displaying different target cullin specificities. Together, these studies reveal the molecular basis for and functional importance of hierarchical expansion of the NEDD8 conjugation system in establishing selective CRL activation."'
GSE14089_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"We determined the gene expression profiles of murine melan-a melanocytes treated with ASP or alpha-MSH over a 4 days time course using genome-wide oligonucleotide microarrays. As expected, the gene expression patterns emphasized the opposing effects of the 2 ligands, and there were significant reductions in expression of numerous melanogenic proteins elicited by ASP, which correlates with its inhibition of pigmentation. However, ASP also unexpectidly modulated the expression of genes involved in various other cellular pathways, including glutathione synthesis and redox metabolism. Many genes up-regulated by ASP are involved in morphogenesis, cell adhesion and ECM-receptor interactions."'
GSE14089_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Treatment with ASP or alpha-MSH was performed for 3 hr, 1 day, 2 days, 3 days and 4 days, in triplicate. Each biological replicate was submitted to a direct hybridization (treated/untreated samples) after coupling with Cy5 or Cy3 and to a reverse dye-swap, leading to 2 replicated hybridization for each biological sample. A total of 6 hybridized arrays was used for each of the 5 time points, for each drug."'
GSE14101_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Leukemias with MLL-rearrangements are characterized by high expression of the homeo box gene MEIS1. In these studies, we knocked down Meis1 expression by shRNA lentivirus transduction in murine Mll-AF9 leukemia cells. Meis1 knockdown resulted in decreased proliferation and survival of murine Mll-AF9 leukemia cells. We also observed reduced clonogenic capacity and increased monocytic differentiation. The establishment of leukemia in transplant recipients was significantly delayed by Meis1 knockdown. Gene expression profiling of cells transduced with Meis1 shRNA showed reduced expression of genes associated with cell cycle entry and progression. shRNA mediated knockdown of MEIS1 in human MLL-fusion gene leukemia cell lines resulted in reduced cell growth. These results show that MEIS1 expression is important for MLL-rearranged leukemias and suggest that MEIS1 promotes cell cycle entry. Targeting MEIS1 may have therapeutic potential for treating leukemias expressing this transcription factor."'
GSE14101_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Murine Mll-AF9 leukemia (4166) cells were transduced with lentivirus expressing shRNA against Meis1 or control lentivirus (empty vector). Gene expression profiles were compared at 48 hours post transduction, using Puromycin as selection agent for transduced cells."'
GSE14201_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"For the stem cell signature we used cell fractions of intestines from Lgr5-EGFP-ires-CreERT2 mice, expressing GFP under the control of the Lgr5 promoter. RNA was isolated from two FACS sorted cell populations, one expressing GFP at high levels (GFPhi) and the other expressing GFP at low levels (GFPlo). For the analysis of Ascl2 target genes RNA was isolated from intestinal epithelial cells of Ah-Cre/Ascl2floxed/floxed animals and Ah-Cre/Ascl2floxed/wt control animals 3 and 5 days post induction. Differentially labelled cRNA from GFPhi and GFPlo cells from two different sorts (each combining three different mice) were hybridised on 4X44K Agilent Whole Mouse Genome dual colour Microarrays (G4122F) in two dye swap experiments, resulting in four individual arrays. For the Ascl2 target gene analysis we analyzed the 3 and 5 days PI experiments in two dye swap experiments, resulting in four individual arrays."'
GSE14226_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We previously identified a novel SNF1/AMPK-related protein kinase, Hunk, from a mammary tumor arising in an MMTV-neu transgenic mouse. The function of this kinase is unknown. Using targeted deletion in mice, we now demonstrate that Hunk is required for the metastasis of c-myc-induced mammary tumors, but is dispensable for normal development. Reconstitution experiments revealed that Hunk is sufficient to restore the metastatic potential of Hunk-deficient tumor cells, as well as defects in migration and invasion, and does so in a manner that requires its kinase activity. Consistent with a role for Hunk in the progression of human cancers, the human homologue of Hunk is overexpressed in aggressive subsets of carcinomas of the ovary, colon, and breast. In addition, a murine gene expression signature that distinguishes Hunk-wild type from Hunk-deficient mammary tumors predicts clinical outcome in women with breast cancer. Together, these findings establish a role for Hunk in metastasis and an in vivo function for this kinase."'
GSE14236_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The tumorigenesis capacity of MLL-AF4 alone is insufficient for causing leukemia. Based on the finding that an Flt3 gene mutation in the tyrosine kinase domain (TKD) was observed in approximately 15% of MLL leukemia, we investigated synergistic leukemogenesis effects of the two genes in vitro. In a mouse IL3-dependent cell line, 32Dc, the expression of MLL-AF4 and Flt3 TKD was induced using a lentiviral vector. We performed gene expression profiling in the MLL-AF4 and the Flt3 TKD+MLL-AF4 expressing 32Dc cells. The enhancement of Hox genes expression was not identified. However, instead, the expression of S100A6, which was involved in the control of cell proliferation, was synergistically enhanced in the presence of both MLL-AF4 and Flt3 TKD genes."'
GSE14236_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"The tumorigenesis capacity of MLL-AF4 alone is insufficient for causing leukemia. Based on the finding that an Flt3 gene mutation in the tyrosine kinase domain (TKD) was observed in approximately 15% of MLL leukemia, we investigated synergistic leukemogenesis effects of the two genes in vitro. In a mouse IL3-dependent cell line, 32Dc, the expression of MLL-AF4 and Flt3 TKD was induced using a lentiviral vector. We performed gene expression profiling in the MLL-AF4 and the Flt3 TKD+MLL-AF4 expressing 32Dc cells. The enhancement of Hox genes expression was not identified. However, instead, the expression of S100A6, which was involved in the control of cell proliferation, was synergistically enhanced in the presence of both MLL-AF4 and Flt3 TKD genes."'
GSE14236_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"We performed gene expression profiling: 32Dc vs. MLL-AF4 expressing 32Dc, 32Dc vs. Flt3 TKD+MLL-AF4 expressing 32Dc, and MLL-AF4 expressing 32Dc vs. Flt3 TKD+MLL-AF4 expressing 32Dc. A single sample for each expressing cells was analyzed."'
GSE14242_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We used gene array analysis of cortical bone to identify Phex-dependent gene transcripts regulating Fgf23 production and mineralization in Hyp mice. We discovered that activation of Fgf receptor- and Wnt-pathways contribute to increased Ffg23 gene transcription in Hyp bone. We found evidence in Hyp bone for increased expression of Fgf1, Fgf7, and Egr2 in the Fgf-signaling pathway and decrements in Sost and Cpz and increments in Sfrp1 and 4 in the Wnt-signaling pathway. Moreover, activation of Fgf and Wnt-signaling stimulated, whereas Tgf β inhibited Fgf23 promoter activity in osteoblasts. We also observed reductions in Bmp1, a metalloproteinase that metabolizes the Fgf23 regulatory extracellular matrix protein Dmp1. These findings suggest that elevation of Fgf23 expression in osteocytes is regulated by interactions between cell surface expression of Phex, extracellular matrix proteins and paracrine effects of Fgf and Wnt. Alterations were also found in enzymes regulating the posttranslational processing and stability of Fgf23, including decrements in the glycosyltransferase Galnt3 and the proprotein convertase Pcsk5. In addition, we found that the Pcsk5 and the glycosyltransferase Galnt3 were decreased in Hyp bone, suggesting that reduced post-translational processing of FGF23 may also contribute to increased Fgf23 levels in Hyp mice. With regards to mineralization, we identified additional candidates to explain the intrinsic mineralization defect in Hyp osteoblasts, including increases in the mineralization inhibitors Mgp and Thbs4, as well as increases in local pH altering factors, carbonic anhydrase 12 (Car12) and 3 (Car3) and the sodium-dependent citrate transporter (Slc13a5). These studies demonstrate the complexity of gene expression alterations in bone that accompanies inactivating Phex mutations and identify novel pathways that may coordinate Fgf23 expression and mineralization of extracellular matrix in Hyp bone."'
GSE14242_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"We used gene array analysis of cortical bone to identify Phex-dependent gene transcripts regulating Fgf23 production and mineralization in Hyp mice. We discovered that activation of Fgf receptor- and Wnt-pathways contribute to increased Ffg23 gene transcription in Hyp bone. We found evidence in Hyp bone for increased expression of Fgf1, Fgf7, and Egr2 in the Fgf-signaling pathway and decrements in Sost and Cpz and increments in Sfrp1 and 4 in the Wnt-signaling pathway. Moreover, activation of Fgf and Wnt-signaling stimulated, whereas Tgf β inhibited Fgf23 promoter activity in osteoblasts. We also observed reductions in Bmp1, a metalloproteinase that metabolizes the Fgf23 regulatory extracellular matrix protein Dmp1. These findings suggest that elevation of Fgf23 expression in osteocytes is regulated by interactions between cell surface expression of Phex, extracellular matrix proteins and paracrine effects of Fgf and Wnt. Alterations were also found in enzymes regulating the posttranslational processing and stability of Fgf23, including decrements in the glycosyltransferase Galnt3 and the proprotein convertase Pcsk5. In addition, we found that the Pcsk5 and the glycosyltransferase Galnt3 were decreased in Hyp bone, suggesting that reduced post-translational processing of FGF23 may also contribute to increased Fgf23 levels in Hyp mice. With regards to mineralization, we identified additional candidates to explain the intrinsic mineralization defect in Hyp osteoblasts, including increases in the mineralization inhibitors Mgp and Thbs4, as well as increases in local pH altering factors, carbonic anhydrase 12 (Car12) and 3 (Car3) and the sodium-dependent citrate transporter (Slc13a5). These studies demonstrate the complexity of gene expression alterations in bone that accompanies inactivating Phex mutations and identify novel pathways that may coordinate Fgf23 expression and mineralization of extracellular matrix in Hyp bone."'
GSE14243_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"As4.1 cells are a renin-expressing cell line commonly used to study the molecular regulation of the mouse renin gene.  In the present study, the global gene expression profile was assessed in these cells under control conditions (VEHICLE) and after treatment with interleukin (IL) or hydrogen peroxide (HP), both of which negatively regulate mouse renin gene expression."'
GSE14243_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"For each experimental group, 2 separate cultures of As4.1 cells were used.  Cells were treated with interleukin (IL), hydrogen peroxide (HP) or vehicle control (VEHICLE). Cellular RNA was prepared using conventional methods and quality was assessed using the Bioanalyzer 2100 (Agilent Technologies).  All the microarray procedures were conducted at the University of Iowa DNA Core facility using standard Affymetrix protocols.  In brief, approximately 5 ug of total RNA was used as input to a one-step amplification procedure to generate biotin-labeled RNA fragments for hybridization to the Affymetrix GeneChip Mouse Genome 430 2.0 array."'
GSE14249_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Genes induced by IL-9 in the colon of transgenic mice"'
GSE14249_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The aim of this work was to identify genes induced by IL-9 in the colon of IL-9-tarnsgenic mice (Tg5). Therefore, we performed a comprehensive study of the genes expressed in the colon of IL-9 transgenic and wild type FVB mice, taking advantage of the affymetrix microarray technology."'
GSE14249_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Keywords: cytokine-induced response"'
GSE14267_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Cardiac hypertrophy can lead to heart failure, and is induced either by physiological stimuli eg postnatal development, chronic exrcise training or pathological stimuli eg pressure or volume overload. This data set looks at microRNA profiles in mouse models to examine whether phosphoinositide 3-kinase (p110 alpha isoform) activity is critical for the maintenance of cardiac function and long term survival in a seeting of heart failure (myocardial infarction). The significance and expected outcome are to recognise genes involved in models of heart failure and attempt to examine underlying regulator pathways involved in possible cardica maintenance in the PI3K mouse model. The matching mRNA gene expression profile (GSE7487) is examined to look for mRNA and microRNA interactions."'
GSE14268_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"There are up to three biological replicates (indicated by 1, 2, and 3) of primary hippocampal neurons from new born rats and the cerebellum and hippocampus regions from adult mice treated for three days (control, morphine, and fentanyl).  The biological replicates were from experiments performed on different dates.  Each biological replicate contained cells or tissues collected from multiple animals so that enough RNA could be extracted for RNA analysis.  RNA was labelled with a green dye, mixed with a reference DNA sample labelled with a red dye.  The reference DNA contained a number of synthetic DNA oligos with mature microRNA sequences that served to verify microarray hybridization.  RNA signals were in ch1, DNA signals ch2."'
GSE14277_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Here, we report findings with a transgenic disease model where targeted expression of c-raf to respiratory epithelium induced adenocarcinomas. Specifically, by use of laser microdissection we harvested either tumor or transgenic and non-transgenic but otherwise morphologically unaltered cells. We then searched genome wide for regulated genes and validated results by quantitative real-time PCR. Overall, 473 and 541 genes were significantly regulated when cancer versus transgenic and cancer versus non-transgenic cells were compared. Principal component analysis and hierarchical clustering of the data clearly separated the cancer cells from transgenic and non-transgenics and we observed predominately repression of gene expression at advanced stages of tumor growth. Nonetheless genes up-regulated in dysplasia were also up-regulated in solid tumors. We observed groups of genes acting in concert either linked to development with an unexpected high number of genes coding either for the epithelial mesenchymal or mesenchymal endothelial transition. Additionally, genes coding for cell adhesion including the integrins and the tight and gap junction proteins were repressed (integrin alpha 1, integrin alpha 8, claudin 2, claudin 5, gap junction membrane channel protein alpha 5 and cadherin 5) but ligands for the membrane bound epidermal growth factor tyrosine kinase i.e. epi- and amphiregulin were up-regulated. Moreover, molecules in the signalling of vascular endothelial growth factor receptor- 2 and VEGFD, Notch and WNT were regulated as were glycosylases that facilitate cellular recognition. Other regulated signalling molecules included exchange factor such as RAP guanine nucleotide exchange factor 3, RHO guanine nucleotide exchange factor 10, RAS guanine releasing protein 2 and 3, and RAS guanine nucleotide-releasing factor 1 that play a role in an activation of the MAP kinases."'
GSE14277_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Here, we report findings with a transgenic disease model where targeted expression of c-raf to respiratory epithelium induced adenocarcinomas. Specifically, by use of laser microdissection we harvested either tumor or transgenic and non-transgenic but otherwise morphologically unaltered cells. We then searched genome wide for regulated genes and validated results by quantitative real-time PCR. Overall, 473 and 541 genes were significantly regulated when cancer versus transgenic and cancer versus non-transgenic cells were compared. Principal component analysis and hierarchical clustering of the data clearly separated the cancer cells from transgenic and non-transgenics and we observed predominately repression of gene expression at advanced stages of tumor growth. Nonetheless genes up-regulated in dysplasia were also up-regulated in solid tumors. We observed groups of genes acting in concert either linked to development with an unexpected high number of genes coding either for the epithelial mesenchymal or mesenchymal endothelial transition. Additionally, genes coding for cell adhesion including the integrins and the tight and gap junction proteins were repressed (integrin alpha 1, integrin alpha 8, claudin 2, claudin 5, gap junction membrane channel protein alpha 5 and cadherin 5) but ligands for the membrane bound epidermal growth factor tyrosine kinase i.e. epi- and amphiregulin were up-regulated. Moreover, molecules in the signalling of vascular endothelial growth factor receptor- 2 and VEGFD, Notch and WNT were regulated as were glycosylases that facilitate cellular recognition. Other regulated signalling molecules included exchange factor such as RAP guanine nucleotide exchange factor 3, RHO guanine nucleotide exchange factor 10, RAS guanine releasing protein 2 and 3, and RAS guanine nucleotide-releasing factor 1 that play a role in an activation of the MAP kinases."'
GSE14277_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Taken collectively, our study provides valuable information for new candidate genes in lung adenocarcinoma induced by exaggerted c-raf kinase activity."'
GSE14288_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy."'
GSE14288_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy."'
GSE14288_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy."'
GSE14288_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy."'
GSE14288_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy."'
GSE14290_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Measuring global gene expression using cDNA or oligonucleotide microarrays is an effective approach to understanding the complex mechanisms of the effects of radiation. However, few studies have been carried out that investigate gene expression in vivo after prolonged exposure to low-dose-rate radiation. In this study, C57BL/6J mice were continuously irradiated with γ-rays for 485 days at dose-rates of 0.032 – 13 μGy/min. Gene expression profiles in the kidney and testis from irradiated and unirradiated mice were analyzed, and differentially expressed genes were identified. A combination of pathway analysis and hierarchical clustering of differentially expressed genes revealed that expression of genes involved in mitochondrial oxidative phosphorylation was elevated in the kidney after irradiation at the dose-rates of 0.65 μGy/min and 13 μGy/min. Expression of cell cycle-associated genes was not profoundly modulated in the kidney, in contrast to the response to acute irradiation, suggesting a threshold in the dose-rate for modulation of the expression of cell cycle-related genes in vivo following exposure to radiation. We demonstrated that changes to the gene expression profile in the testis were largely different from those in the kidney. The Gene Ontology categories “DNA metabolism”, “response to DNA damage” and “DNA replication” overlapped significantly with the clusters of genes whose expression decreased with an increase in the dose-rate to the testis. These observations provide a fundamental insight into the organ-specific responses to low-dose-rate radiation."'
GSE14293_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Phagocytosis represents a mechanism used by macrophages to remove pathogens and cellular debris. Recent evidence suggested that amino acid or glucose deprivation may cause an increase in phagocytosis of heat-inactivated Escherichia coli and Staphylococcus aureus by macrophages, but not the uptake of platelets, apoptotic cells or beads. Increased phagocytosis of bacteria could be blocked by phagocytosis inhibitors and depended on p38 MAP kinase activity. To examine potentially important downstream pathways linked to EBSS-induced starvation and p38 MAP kinase activation, a full genome microarray representing over 41,000 mouse genes or transcripts was probed with cDNA isolated from J774A.1 macrophages that were treated with EBSS, EBSS supplemented with the p38 inhibitor SB202190 or control medium supplemented with 10% fetal bovine serum."'
GSE14293_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Phagocytosis represents a mechanism used by macrophages to remove pathogens and cellular debris. Recent evidence suggested that amino acid or glucose deprivation may cause an increase in phagocytosis of heat-inactivated Escherichia coli and Staphylococcus aureus by macrophages, but not the uptake of platelets, apoptotic cells or beads. Increased phagocytosis of bacteria could be blocked by phagocytosis inhibitors and depended on p38 MAP kinase activity. To examine potentially important downstream pathways linked to EBSS-induced starvation and p38 MAP kinase activation, a full genome microarray representing over 41,000 mouse genes or transcripts was probed with cDNA isolated from J774A.1 macrophages that were treated with EBSS, EBSS supplemented with the p38 inhibitor SB202190 or control medium supplemented with 10% fetal bovine serum."'
GSE14293_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Phagocytosis represents a mechanism used by macrophages to remove pathogens and cellular debris. Recent evidence suggested that amino acid or glucose deprivation may cause an increase in phagocytosis of heat-inactivated Escherichia coli and Staphylococcus aureus by macrophages, but not the uptake of platelets, apoptotic cells or beads. Increased phagocytosis of bacteria could be blocked by phagocytosis inhibitors and depended on p38 MAP kinase activity. To examine potentially important downstream pathways linked to EBSS-induced starvation and p38 MAP kinase activation, a full genome microarray representing over 41,000 mouse genes or transcripts was probed with cDNA isolated from J774A.1 macrophages that were treated with EBSS, EBSS supplemented with the p38 inhibitor SB202190 or control medium supplemented with 10% fetal bovine serum."'
GSE14316_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"The cytokine IL-10 deactivates macrophages and has been shown to impair resistance to mycobacterial infection. We have infected transgenic mice overexpressing IL-10 under control of the macrophage-specific CD68 promoter (macIL-10tg mice) with Mycobacterium tuberculosis by aerosol and found increased bacterial loads in the lungs of macIL-10tg mice."'
GSE14320_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Basal and kainate-induced gene expression in A-CREB mouse hippocampi"'
GSE14320_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The cAMP responsive element binding protein (CREB) pathway has been involved in two major cascades of gene expression regulating neuronal function. The first one presents CREB as a critical component of the molecular switch that control longlasting forms of neuronal plasticity and learning. The second one relates CREB to neuronal survival and protection. To investigate the role of CREB-dependent gene expression in neuronal plasticity and survival in vivo, we generated bitransgenic mice expressing A-CREB, an artificial peptide with strong and broad inhibitory effect on the CREB family, in forebrain neurons in a regulatable manner. The expression of ACREB in hippocampal neurons impaired L-LTP, reduced intrinsic excitability and the susceptibility to induced seizures, and altered both basal and activity-driven gene expression. In the long-term, the chronic inhibition of CREB function caused severe loss of neurons in the CA1 subfield as well as in other brain regions. Our experiments confirmed previous findings in CREB deficient mutants and revealed new aspects of CREB-dependent gene expression in the hippocampus supporting a dual role for CREB-dependent gene expression regulating intrinsic and synaptic plasticity and promoting neuronal survival. manufacturer's protocol."'
GSE14320_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"The cAMP responsive element binding protein (CREB) pathway has been involved in two major cascades of gene expression regulating neuronal function. The first one presents CREB as a critical component of the molecular switch that control longlasting forms of neuronal plasticity and learning. The second one relates CREB to neuronal survival and protection. To investigate the role of CREB-dependent gene expression in neuronal plasticity and survival in vivo, we generated bitransgenic mice expressing A-CREB, an artificial peptide with strong and broad inhibitory effect on the CREB family, in forebrain neurons in a regulatable manner. The expression of ACREB in hippocampal neurons impaired L-LTP, reduced intrinsic excitability and the susceptibility to induced seizures, and altered both basal and activity-driven gene expression. In the long-term, the chronic inhibition of CREB function caused severe loss of neurons in the CA1 subfield as well as in other brain regions. Our experiments confirmed previous findings in CREB deficient mutants and revealed new aspects of CREB-dependent gene expression in the hippocampus supporting a dual role for CREB-dependent gene expression regulating intrinsic and synaptic plasticity and promoting neuronal survival. manufacturer's protocol."'
GSE14326_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The vertebrate-specific transcription factor RE-1 silencing transcription factor or neuron-restrictive silencer factor (REST/NRSF) was first described as a negative regulator restricting expression of neuronal genes to neurons in a variety of genetic contexts. However, REST/NRSF has a more general role in the regulation of gene expression that involves chromatin remodelling via a SWI/SNF complex. We identified a 677 gene repertoire of potential REST/NRSF-dependent genes taking advantage of Rest/Nrsf gene silencing in a mouse cell line. Using Ka/Ks analysis, we found that REST/NRSF protein, REST/NRSF interactors and the products of REST/NRSF-dependent genes display significantly higher rates of protein evolution in primates than in rodents. The McDonald-Kreitman test indicated positive selection for human REST/NRSF and nuclear RNA-binding proteins encoded by REST/NRSFdependent genes. In these proteins, we demonstrated sites under positive selection within the primate’s clade. Importantly, the REST/NRSF-dependent gene repertoire is statistically enriched in genes disrupted in neuropsychiatric diseases such as schizophrenia. In addition, we found that Smarca2 (Brm), Smarcd3 (Baf60c), Smarce1 (Baf57), Hdac1, RcoR1, and Mecp2, which are part of the REST/NRSFSWI/SNF chromatin remodelling complex, are transcriptionally regulated by REST/NRSF. Changing their gene dosage in vitro induced abnormal dendritic and dendritic spine phenotypes that were previously observed in rodent models of neuropsychiatric diseases. Altogether, these results suggest that genes encoding proteins of the REST/NRSF-SWI/SNF pathway display primate-specific accelerated"'
GSE14326_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_overall_design	"Agilent Whole Mouse Genome oligomicroarrays (GEO accession no. GPL2872, Agilent Technologies, Palo Alto, CA) were used. They contain 60-mer DNA probes synthesized in situ in a 44k format. Of 44,290 spots, 2756 are controls. The remaining 41,534 spots represent 33,661 unique transcripts which correspond to 20,202 unique human genes. Six independent (NRSF silencing overexpression, six individual samples) measurements were carried out for each group of biological conditions using exchanged dye-labeled RNA targets (i.e., Cy3 and Cy5 dyeswapping experiments)."'
GSE14339_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Our previous studies have implicated CHIP as a co-chaperone/ubiquitin ligase, whose activities yield protection against stress-induced apoptotic events. In this report, we demonstrate a stress-dependent interaction between CHIP (carboxyl terminus of Hsp70-interacting protein) and Daxx, death domain-associated protein. This interaction interferes with the stress-dependent association of HIPK2 with Daxx, blocking phosphorylation of serine 46 in p53 and inhibiting the p53-dependent apoptotic program. Microarray analysis confirmed suppression of the p53-dependent transcriptional portrait in CHIP (+/+) but not in CHIP (-/-) heat shocked MEFs. The interaction between CHIP and Daxx results in ubiquitination of Daxx which is then partitioned to an insoluble compartment of the cell. In vitro ubiquitination of Daxx by CHIP revealed that Ub chain formation utilizes non canonical lysine linkages associated with resistance to proteasomal degradation. CHIP's ubiquitination of Daxx utilizes lysines 630 and 631 and competes with the cell's sumoylation machinery at these residues. These studies implicate CHIP as a stress-dependent regulator of Daxx that counters Daxx's pro-apoptotic influence in the cell. By abrogating p53-dependent apoptotic pathways and by ubiquitination competitive with Daxx sumoylation, CHIP integrates the cell's proteotoxic stress response with cell cycle pathways that influence cell survival."'
GSE14350_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Interleukin-2 receptor (IL-2R) signaling is essential for T regulatory (Treg) cell development and homeostasis. Here we show that expression of IL-2Rbeta chains that lack tyrosine residues important for the association of the adaptor Shc and the transcription factor STAT5 in IL-2Rbeta-deficient mice resulted in production of a normal proportion of natural Treg cells that suppressed severe autoimmunity related with deficiency in IL-2 or IL-2R. These mutant IL-2Rbeta chains supported suboptimal and transient STAT5 activation that upregulate the transcription factor Foxp3 to normal amounts in natural, but not induced, Treg cells. Using cells T cell obtained from normal C57BL/6 mice and mice harboring Treg cells with impaired IL-2R signaling, gene expression profiling revealed many targets in peripheral natural Treg cells that were IL-2-dependent and a substantial overlap between the Treg cell IL-2-dependent gene program and the Treg cell transcriptional signature. Collectively, these findings demonstrate that a critical, and perhaps minor, subset of IL-2-dependent targets in Treg cells is indexed to a low IL-2R signaling threshold and that a substantial proportion of the Treg cell gene program is regulated by IL-2. CD4 T effector cells also showed many IL-2R-dependent gene and these also overlapped in a distintive manner with the IL-2-dependent genes of Treg cells and the Treg gene signature."'
GSE14350_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Interleukin-2 receptor (IL-2R) signaling is essential for T regulatory (Treg) cell development and homeostasis. Here we show that expression of IL-2Rbeta chains that lack tyrosine residues important for the association of the adaptor Shc and the transcription factor STAT5 in IL-2Rbeta-deficient mice resulted in production of a normal proportion of natural Treg cells that suppressed severe autoimmunity related with deficiency in IL-2 or IL-2R. These mutant IL-2Rbeta chains supported suboptimal and transient STAT5 activation that upregulate the transcription factor Foxp3 to normal amounts in natural, but not induced, Treg cells. Using cells T cell obtained from normal C57BL/6 mice and mice harboring Treg cells with impaired IL-2R signaling, gene expression profiling revealed many targets in peripheral natural Treg cells that were IL-2-dependent and a substantial overlap between the Treg cell IL-2-dependent gene program and the Treg cell transcriptional signature. Collectively, these findings demonstrate that a critical, and perhaps minor, subset of IL-2-dependent targets in Treg cells is indexed to a low IL-2R signaling threshold and that a substantial proportion of the Treg cell gene program is regulated by IL-2. CD4 T effector cells also showed many IL-2R-dependent gene and these also overlapped in a distintive manner with the IL-2-dependent genes of Treg cells and the Treg gene signature."'
GSE14361_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells. "'
GSE14361_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells. "'
GSE14361_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells. "'
GSE14361_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells. "'
GSE14361_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"cDNA microarray analysis was performed on sorted Lin neg, cKit+, CD150+, CD48neg HSCs from IFNα treated (16h after treatment) and untreated (littermate) mice. Per condition 3 independent biological replicates were analysed. "'
GSE14363_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"We studied the role of the cAMP responsive factor CREB in promoting insulin resistance following its activation in adipose under obese conditions"'
GSE14363_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"We identified genes that were upregulated in primary cultures of mouse adipocytes following exposure to forskolin; and we characterized genes that are also induced in white adipose tissue in mice maintained on a  high fat diet."'
GSE14363_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We identified genes that were upregulated in primary cultures of mouse adipocytes following exposure to forskolin; and we characterized genes that are also induced in white adipose tissue in mice maintained on a  high fat diet."'
GSE14365_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Aire is an important transcription regulator that mediates a role in central tolerance via promoting the promiscuous expression of tissue-specific antigens in the thymus. Although several mouse models of Aire-deficiency have been described, none has analysed the phenotype induced by a mutation that emulates the common 13bp deletion in human APECED by disrupting the first PHD domain in exon 8. Aire-deficient mice with a corresponding mutation showed some disturbance of the medullary epithelial compartment, but at the phenotypic level their T cell compartment appeared relatively normal in the thymus and periphery. An increase in the number of activated T cells was evident, and autoantibodies against several organs were detected. At the histological level, lymphocytic infiltration of several organs indicated the development of autoimmunity, though symptoms were mild and quality of life for Aire-deficient mice appeared equivalent to wild-type littermates, with the exception of male infertility. Vbeta and CDR3 length analysis suggested that each Aire-deficient mouse developed it own polyclonal autoimmune repertoire. Finally, given the prevalence of candidiasis in APECED patients, we examined the control of infection with Candida albicans in Aire-deficient mice. No increase in disease susceptibility was found for either oral or systematic infection. These observations support the view that additional genetic and/or environmental factors contribute substantially to the overt nature of autoimmunity associated with Aire mutations, even for mutations identical to those found in humans with APECED."'
GSE14366_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Neuroprotective therapies for retinal degeneration may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning stabilizes the transcription factor HIF-1α in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration."'
GSE14367_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Schistosomiasis continues to be an important cause of parasitic morbidity and mortality world-wide. Determining the molecular mechanisms regulating the development of granulomas and fibrosis will be essential for understanding how schistosome antigens interact with the host environment. We report here the first whole genome microarray analysis of the murine liver during the progression of Schistosoma japonicum egg-induced granuloma formation and hepatic fibrosis. Our results reveal a distinct temporal relationship between the expression of chemokine subsets and the recruitment of cells to the infected liver. Genes up-regulated earlier in the response included T- and B-cell chemoattractants, reflecting the early recruitment of these cells illustrated by flow cytometry. The later phases of the response corresponded with peak recruitment of eosinophils, neutrophils, macrophages and myofibroblasts/hepatic stellate cells (HSCs) and the expression of chemokines with activity for these cells including CCL11 (eotaxin 1), members of the Monocyte-chemoattractant protein family (CCL7, CCL8, CCL12) and the Hepatic Stellate Cell/Fibrocyte chemoattractant CXCL1. Peak expression of macrophage chemoattractants (CCL6, CXCL14) and markers of alternatively-activated macrophages (e.g. Retnla) during this later phase provides further evidence of a role for these cells in schistosome-induced pathology. Additionally, we demonstrate that CCL7 immunolocalises to the fibrotic zone of granulomas. Furthermore, striking up-regulation of neutrophil markers and the localisation of neutrophils and the neutrophil chemokine S100A8 to fibrotic areas suggests the involvement of neutrophils in S. japonicum¬-induced hepatic fibrosis. These results further our understanding of the immunopathogenic and, especially, chemokine signalling pathways that regulate the development of S. japonicum-induced granulomas and fibrosis and may provide correlative insight into the pathogenesis of other chronic inflammatory diseases of the liver where fibrosis is a common feature."'
GSE14375_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Culture induced changes in Blood-Brain Barrier transcriptome: implications for amino acid transporters in vivo"'
GSE14375_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Tight homeostatic control of brain amino acids (AA) depends on transport via solute family carrier proteins expressed by the Blood-Brain Barrier (BBB) microvascular endothelial cells (BMEC). To characterize the mouse BMEC transcriptome and probe culture-induced changes microarray analyses of PECAM-1+ endothelial cells (ppMBMECs) were compared with primary MBMECs (pMBMEC) cultured in the presence or absence of glial cells, and with b.End5 endothelioma cell-line. Selected cell marker and AA transporter mRNA levels were further verified by real-time RT PCR."'
GSE14381_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study.  An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus.  Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, I; alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL.  Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE14381_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study.  An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus.  Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, I; alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL.  Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE14391_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study. An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus. Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, I; alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL. Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE14391_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study. An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus. Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, I; alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL. Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE14391_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Adult male Swiss Webster mice (30-35 g) were anesthetized, a bipolar electrode was implanted adjacent to the sciatic nerve and the hindlimb immobilized. The voltage-force relation was determined to establish supramaximal stimulation conditions and the length-tension relation was determined to set the resting length for maximum twitch tension. Contractions were induced by sciatic nerve stimulation (0.5 msec duration, 2-5 volts). The muscles were allowed to rest 15 minutes for full metabolic recovery at physiologic temperatures. Supramaximal stimulation was applied at a rate of 10 Hz for 4 hours. At the end of each experiment the soleus muscles were carefully dissected and flash frozen in liquid nitrogen for analysis of mRNA expression via microarray analysis. The contralateral, unstimulated Soleus provided a genetically matched, paired control for each specimen."'
GSE14395_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Most metabolic studies are conducted in male animals; thus, the molecular mechanism controlling gender-specific pathways has been neglected, including sex-dependent responses to peroxisome proliferator-activated receptors (PPARs). Here we show that PPARalpha has broad female-dependent repressive actions on hepatic genes involved in steroid metabolism and inflammation. In males, this effect is reproduced by the administration of synthetic PPARalpha ligand. Using the steroid hydroxylase gene Cyp7b1 as a model, we elucidated the molecular mechanism of this PPARalpha-dependent repression. Initial sumoylation of the ligand-binding domain of PPARalpha triggers the interaction of PPARalpha with the GA-binding protein alpha bound to the target promoter. Histone deacetylase is then recruited, and histones and adjacent Sp1-binding site are methylated. These events result in the loss of Sp1-stimulated expression, and thus the down-regulation of Cyp7b1. Physiologically, this repression confers protection against estrogen-induced intrahepatic cholestasis, paving the way for a novel therapy against the most common hepatic disease during pregnancy."'
GSE14395_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Most metabolic studies are conducted in male animals; thus, the molecular mechanism controlling gender-specific pathways has been neglected, including sex-dependent responses to peroxisome proliferator-activated receptors (PPARs). Here we show that PPARalpha has broad female-dependent repressive actions on hepatic genes involved in steroid metabolism and inflammation. In males, this effect is reproduced by the administration of synthetic PPARalpha ligand. Using the steroid hydroxylase gene Cyp7b1 as a model, we elucidated the molecular mechanism of this PPARalpha-dependent repression. Initial sumoylation of the ligand-binding domain of PPARalpha triggers the interaction of PPARalpha with the GA-binding protein alpha bound to the target promoter. Histone deacetylase is then recruited, and histones and adjacent Sp1-binding site are methylated. These events result in the loss of Sp1-stimulated expression, and thus the down-regulation of Cyp7b1. Physiologically, this repression confers protection against estrogen-induced intrahepatic cholestasis, paving the way for a novel therapy against the most common hepatic disease during pregnancy."'
GSE14411_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation."'
GSE14412_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation."'
GSE14413_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"Gene expression profiling of interferon-beta stimulated cells"'
GSE14413_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Cytoplasmic DNA triggers the activation of the innate immune system. While downstream signaling components have been characterized, the DNA sensing components remain largely elusive. We performed a systematic proteomics screen for proteins that associate with DNA, traversed to a screen for IFN-β-induced transcripts. We identified DSIRE (DNA sensor for the IL-1β response, previously called AIM2) as a candidate cytoplasmic sensor. DSIRE showed a marked selectivity for double-stranded DNA. DSIRE can recruit the inflammasome adaptor ASC and gets redistributed to ASC speckles upon coexpression of ASC. RNAi-mediated reduction of DSIRE expression led to an impairment in IL-1β maturation. Reconstitution of unresponsive cells with DSIRE, ASC, caspase 1 and IL-1β showed that DSIRE is sufficient for inflammasome activation. Overall, our data strongly suggest that DSIRE is a cytoplasmic DNA sensor for the inflammasome."'
GSE14413_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Cytoplasmic DNA triggers the activation of the innate immune system. While downstream signaling components have been characterized, the DNA sensing components remain largely elusive. We performed a systematic proteomics screen for proteins that associate with DNA, traversed to a screen for IFN-β-induced transcripts. We identified DSIRE (DNA sensor for the IL-1β response, previously called AIM2) as a candidate cytoplasmic sensor. DSIRE showed a marked selectivity for double-stranded DNA. DSIRE can recruit the inflammasome adaptor ASC and gets redistributed to ASC speckles upon coexpression of ASC. RNAi-mediated reduction of DSIRE expression led to an impairment in IL-1β maturation. Reconstitution of unresponsive cells with DSIRE, ASC, caspase 1 and IL-1β showed that DSIRE is sufficient for inflammasome activation. Overall, our data strongly suggest that DSIRE is a cytoplasmic DNA sensor for the inflammasome."'
GSE14413_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"In a genomic screen, we used NIH3T3, L929 and RAW264.7 cells to identify genes that were transcriptionally regulated by IFN-β. We stimulated the cells with IFN-β for 4h, isolated the RNA and analyzed global changes in gene expression by microarray analysis. Overall, 225 genes were upregulated at least 3fold, among which numerous well-known interferon-induced genes were found"'
GSE14413_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"In a genomic screen, we used NIH3T3, L929 and RAW264.7 cells to identify genes that were transcriptionally regulated by IFN-β. We stimulated the cells with IFN-β for 4h, isolated the RNA and analyzed global changes in gene expression by microarray analysis. Overall, 225 genes were upregulated at least 3fold, among which numerous well-known interferon-induced genes were found"'
GSE14414_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation."'
GSE14415_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Gene expression profiling of natural and induced regulatory T cells"'
GSE14415_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The gene expression profile of peripheral Foxp3+ natural regulatory T cells isolated from Foxp3/EGFP bicistronic mice was compared to that of in vitro-induced regulatory T cells and to CD4+ conventional (Foxp3-) T cells. The role of the regulatory T cell transcription factor Foxp3 in shaping the transcriptosomes of natural and induced regulatory T cells was analyzed using mice expressing a mutant FOXP3-EGFP fusion protein (Foxp3deltaEGFP)."'
GSE14415_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"The gene expression profile of peripheral Foxp3+ natural regulatory T cells isolated from Foxp3/EGFP bicistronic mice was compared to that of in vitro-induced regulatory T cells and to CD4+ conventional (Foxp3-) T cells. The role of the regulatory T cell transcription factor Foxp3 in shaping the transcriptosomes of natural and induced regulatory T cells was analyzed using mice expressing a mutant FOXP3-EGFP fusion protein (Foxp3deltaEGFP)."'
GSE14415_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We used gene expression microarrays to examine the transcriptional programs of natural and induced regulatory T cells and the function of Foxp3 in organizing the transcriptosomes of the respective cell type"'
GSE14415_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Conventional T cells and natural and induced regulatory T cells were derived from Foxp3/EGFP bicistronic mice and analyzed for their gene expression profile. Conventional T cells, regulatory T cell precursors (CD4+Foxp3deltaEGFP+) and induced regulatory T cell precursors (CD4+Foxp3deltaEGFP+) cells were deriv ed from Foxp3deltaEGFP mice"'
GSE14416_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines"'
GSE14416_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Interferon is effective at inducing complete remissions in patients with Chronic Myelogenous Leukemia (CML), and evidence supports an immune mechanism. Here we show that the Type I Interferons (alpha and beta) regulate expression of the Interferon consensus sequence binding protein (ICSBP) in bcr-abl transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of bcr-abl induced leukemia. We identify the chemokines CCL6 and CCL9 as genes prominently induced by the Type I Interferons and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression. Insights into the role of these chemokines in the anti-leukemic response of interferons suggest new strategies for immunotherapy of CML. "'
GSE14416_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Total RNA was isolated from parental BaF3 cells as well as BaF3 cells expressing BCR-ABL, ICSBP, or both BCR-ABL and ICSBP. Using standard Affymetrix protocols the RNA samples were analyzed for gene expression using Affymetrix mouse 430_2 whole genome microarrays arrays. A threshold value of 50 was set for all genes and the list of genes filtered to include only those that had at least one Present flag (""P"" flag) in one of the 4 conditions. For each gene, the ratio of its expression in a particular condition and its expression in parental BaF3 cells was determined. Only genes that had at least a 3-fold up or down change in expression were considered, leaving a set of 1431 genes for further analysis. K-means clustering with Gene cluster 3.0 was used to group these 1431 genes into 15 clusters and JavaTree was used to visualize the results."'
GSE14418_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Cy3: B16F10 mouse melanoma cells, treated by unspecific goat IgG (control) for 2 hours."'
GSE14418_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Cy5: B16F10 mouse melanoma cells, in vitro, treated by an agonist goat polyclonal anti-mouse TIM3 antibody (RnD Systems) for 2 hours."'
GSE14418_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Four biological replicates were used (in this study, biological replicate means different passage numbers of the same cell line). In each case, the treated sample (Cy5) was compared to its control one (Cy3) in Agilent dual-color microarray experiments."'
GSE14421-GPL6462_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study.  An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus.  Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, I; alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL.  Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE14421-GPL6462_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study.  An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus.  Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, I; alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL.  Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE14421-GPL8063_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study.  An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus.  Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, I; alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL.  Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE14421-GPL8063_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Stimulation of the mouse hindlimb via the sciatic nerve was used to induce contractions for 4 hours to investigate acute muscle gene activation in a model of muscle phenotype conversion. Initial force production (1.6 + 0.1 g/g body weight) declined 45% within 10 min and was maintained for the remainder of the experiment. Force returned to initial levels upon completion of the study.  An immediate-early growth response was present in the EDL (FOS, JUN, ATF3, MAFK) with a similar but attenuated pattern in the soleus.  Transcript profiles showed decreased fast fiber specific mRNA (myosin heavy chains 2A, 2B; troponins T3, I; alpha-tropomyosin, m-creatine kinase) and increased slow transcripts (myosin heavy chain slow/1beta, troponin C, tropomyosin 3gamma) in the EDL.  Histological analysis of the EDL revealed glycogen depletion without inflammatory cell infiltration or myofiber damage in stimulated vs. control muscles. Several fiber type specific transcription factors (EYA1, TEAD1, NFATc1 and c4, PPARG, PPARGC1alpha and beta, BHLHB2) increased in the EDL along with transcription factors characteristic of embryogenesis (KLF4, SOX17, TCF15, PKNOX1, ELAV). No established in vivo satellite cell markers or the genes activated during our parallel studies of satellite cell proliferation in vitro (CYCLINS A2, B2, C, E1, MyoD) increased in the stimulated muscles. These data indicated that onset of fast to slow phenotype conversion occurred in the EDL within 4 hours of stimulation without satellite cell recruitment or muscle injury but was driven by phenotype specific transcription factors from resident fiber myonuclei including activation of nascent developmental transcriptional programs."'
GSE14430_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Glis3 mutant mice (Glis3zf/zf) die within the first week after birth due to overt diabetes, evidenced by hyperglycemia and hypoinsulinemia. Histopathological analysis showed that Glis3zf/zf mice develop a pancreatic phenotype with a dramatic loss of beta- (insulin) and delta- (somatostatin) cells contrasting a smaller relative loss of alpha- (glucagon), PP- (pancreatic polypeptide), and epsilon- (ghrelin) cells. Glis3zf/zf mice develop ductal cysts with decreased number of primary cilia, while the acini are not significantly affected. Gene expression profiling by microarray analysis demonstrated that the expression of terminal hormonal genes and several transcription factors important in endocrine development were significantly deregulated in Glis3zf/zf mice. During pancreatic development, Glis3 mRNA expression is induced during the secondary transition, a stage of cell lineage specification and extensive patterning. Changes in pancreatic development of Glis3zf/zf mice are noted during and after this stage; the number of cells staining positively for Ngn3, MafA, or Pdx-1 is greatly diminished. These observations indicate that Glis3 plays a key role in the development of mature beta cells."'
GSE14431_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Simvastatin attenuates lung vascular leak and inflammation in a murine model of radiation-induced lung injury"'
GSE14431_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Background: Microvascular injury and increased vascular leakage are prominent features of the radiation-induced lung injury (RILI) which follows cancer–associated thoracic irradiation. The mechanisms of RILI are incompletely understood and therapeutic strategies to limit RILI are currently unavailable. We established a murine model of radiation pneumonitis in order to assess mechanism-based therapies for RILI-induced inflammation and vascular barrier dysfunction. Based on prior studies, we investigated the therapeutic potential of simvastatin as a vascular barrier protective agent in RILI."'
GSE14431_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Methods: C57BL6/J mice receiving single dose exposure to 18, 20, 22, or 25 Gy, (n=10/group) were temporally assessed (4-12 weeks) for cellular and biochemical indices of injury present in both bronchoalveolar lavage (BAL) and lung tissues (cytokines, tyrosine nitrosylated proteins, leukocytes, extravasation of Evans blue dye or EBD, BAL albumin, histology). In specific experiments, irradiated mice (25Gy) received simvastatin (10 mg/kg) via intraperitoneal injection three times a week (pre and post irradiation) for 2- 6 weeks post irradiation."'
GSE14431_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Results. Acute RILI evolved in a dose- and time-dependent fashion. Mice irradiated with 25Gy exhibited modest increases in BAL leukocytes but significant increases in BAL IL-6 (p=0.03) and TNF-a (p=0.01) at 4 weeks compared to controls. Increases in BAL nitrotyrosine content peaked at 6 weeks (p=0.03) and was accompanied by marked nitrotyrosine immunostaining in lung tissues. Indices of increase lung vascular permeability such as EBD extravasation, BAL protein and BAL albumin significantly increased over time beginning at 6 weeks (p>0.002 all) with histological evidence of severe edema formation and airway inflammation. Simvastatin- treated irradiated mice were noted to exhibit marked attenuation of vascular leak with significantly decreased BAL protein (p=0.01) and inflammatory cell infiltration (50% reduction)."'
GSE14431_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We used microarrays to detail the global programme of gene expression induced by radiation in Wild type and the protection of SIMVA"'
GSE14431_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"animals were treated by Vehical, Radiation (25Gy), SIMVA(10mg/kg), or both."'
GSE14438_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"TIM-3 is known to be expressed on dendritic cells, monocytes, melanoma cells, mast cells and on activated Th1 cells. In activated Th1 cells, stimulating TIM-3 by one of its ligands, galectin-9, leads to apoptosis and thus it plays a central role in terminating Th1-type immune responses. Interestingly, in IgE/antigen-activated mast cells TIM-3 enhances the production of IL-13 and IL-4. To get a more complete picture about the gene expression changes induced by TIM-3 in mast cells, in vitro differentiated mouse immature mast cells were stimulated by an agonist anti-TIM-3 antibody and IgE-sensitized mouse immature mast cells were activated by antigen and an agonist anti-TIM-3 antibody for 2 or 16 hours (overnight)."'
GSE14438_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"TIM-3 is known to be expressed on dendritic cells, monocytes, melanoma cells, mast cells and on activated Th1 cells. In activated Th1 cells, stimulating TIM-3 by one of its ligands, galectin-9, leads to apoptosis and thus it plays a central role in terminating Th1-type immune responses. Interestingly, in IgE/antigen-activated mast cells TIM-3 enhances the production of IL-13 and IL-4. To get a more complete picture about the gene expression changes induced by TIM-3 in mast cells, in vitro differentiated mouse immature mast cells were stimulated by an agonist anti-TIM-3 antibody and IgE-sensitized mouse immature mast cells were activated by antigen and an agonist anti-TIM-3 antibody for 2 or 16 hours (overnight)."'
GSE14438_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Bone marrow cells were differentiated in RPMI + 10% FCS + 5 ng/ml mouse IL-3 + 40 ng/ml mouse SCF for >4 weeks. The purity of the cell cultures was >90% at this time point (FcERIa+/c-kit+ cells). These in vitro-differentiated immature mast cells were then treated by either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml for 2 or 16 hours). For the IgE/antigen-activated mouse mast cells, these in vitro-differentiated immature mast cells were sensitized by 5 ug/ml anti-DNP IgE (Sigma) for 1 hour and then treated with 100 ng/ml DNP-HSA (antigen, Sigma) and either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml) for 2 or 16 hours. The anti-TIM-3 samples were labeled by Cy5 and they were compared to the Cy3-labeled, goat IgG controls in a dual-color, paired experimental setup. The Agilent Whole Mouse Genome 4x44K expression microarray kit and Dual-Color Protocol version 5.5 were used in the experiments."'
GSE14454_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"In a variety of organisms, including mammals, caloric restriction improves metabolic status and lowers the incidence of chronic-degenerative diseases, ultimately leading to increased lifespan. Here we show that knockout mice for Eps8, a regulator of actin dynamics, display reduced bodyweight, partial resistance to age- or diet-induced obesity, and overall improved metabolic status. We present evidence that these phenotypes, which are associated to increased lifespan in the Eps8 null mice, are due to caloric restriction. This, in turn, is caused by reduced intestinal fat absorption, due to altered morphogenesis of microvilli in intestinal enterocytes. In the nematode, genetic removal of Eps8, causes a microvillar phenotype, indistinguishable from that observed in mice, which leads to early larval lethality. By exploiting the nematode model system, we demonstrate here that the actin bundling activity of Eps8 is indispensable for viability and proper intestinal morphogenesis. This result links a precise molecular function of Eps8 to proper microvillar morphogenesis, and therefore to the phenotype of Eps8-null mice. Our results implicate actin dynamics in individual variations in bodyweight, metabolic status and longevity."'
GSE14463_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Methylation profiles of regions, harbouring differentially expressed genes in BMM, were compared between C57BL/6 and BALB/c. Two independently grown, harvested and MCIp treated gDNA preparations were used for each mouse strain (Two biological replicates; One replicate per array). Hypo- and hypermethylated pools serve as diametrically oposed technical replicates (mirror approach)."'
GSE14469_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Expression data from  synovial sarcoma-like tumors induced in a genetically engineered mouse model"'
GSE14469_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Synovial sarcoma-like tumors were generated in mice by conditionally expressing the human t(X;18) translocation-derived SYT-SSX2 fusion protein. Using a Tamoxifen-inducible CreER system, we show here that sporadic expression of SYT-SSX2 across multiple tissue types leads to exclusive formation of synovial sarcoma-like tumors while its widespread expression is lethal.  CreER-based sporadic expression both avoids the severe early developmental phenotypes     associated with widespread SYT-SSX2 expression and better models natural pathogenesis of cancers where transformed cells usually arise within an environment of largely normal cells."'
GSE14469_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Genetically engineered mice capable of conditionally expressing the human synovial sarcoma-associated SYT-SSX2 fusion oncogene were mated with genetically engineered mice expressing the CreER fusion protein from ROSA locus. The progenies harboring both CreER and SYT-SSX2 were followed up with or without tamoxifen injection. Tumors were generated in these mice that were dissected out, RNA extracted, and subjected to expression profiling by microarray analysis."'
GSE14470_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Medulloblastomas (MBs) are the most common brain tumors in children.  Some are thought to originate from cerebellar granule neuron progenitors (GNPs) that fail to undergo normal cell cycle exit and differentiation.  Since microRNAs regulate numerous aspects of cellular physiology and development, we reasoned that alterations in miRNA expression might contribute to MB.  We tested this hypothesis using two spontaneous mouse MB models with specific initiating mutations, Ink4c-/-; Ptch1+/- and Ink4c-/-; p53-/-.  We found that 26 miRNAs showed increased expression and 24 miRNAs showed decreased expression in proliferating mouse GNPs and MBs relative to mature mouse cerebellum, regardless of genotype.  Among the 26 overexpressed miRNAs, nine were encoded by the miR-17~92 cluster family, a group of microRNAs implicated as oncogenes in several tumor types.  Analysis of human MBs demonstrated that three miR-17~92 cluster miRNAs (miR-92, miR-19a and miR-20) were also overexpressed in human MBs with a constitutively activated SHH signaling pathway, but not in other forms of the disease.  To test whether the miR-17~92 cluster could promote MB formation, we enforced expression of these miRNAs in GNPs isolated from cerebella of postnatal (P) day P6 Ink4c-/-; Ptch1+/- mice.  These, but not similarly engineered cells from Ink4c-/-; p53-/- mice, formed MBs in orthotopic transplants with complete penetrance.  Interestingly, orthotopic mouse tumors ectopically expressing miR-17~92 lost expression of the wild-type Ptch1 allele.  Our findings suggest a functional collaboration between the miR-17~92 cluster and the SHH signaling pathway in the development of MBs in mouse and man."'
GSE14499_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"We examined transgenic (TG) mice expressing human APP695 bearing the double Swedish (671KM>NL) and Indiana (717V>F) amyloid precursor protein (APP) mutations. Lentiviral vectors constitutively expressing BDNF-GFP under control of the CMV/ß-actin hybrid promoter or GFP alone were injected into the entorhinal cortices of TG mice bilaterally at age 6 months, a time point by which neuropathological degeneration and cell loss are established. Age-matched wild-type littermates underwent sham surgery or injection of lentivirus expressing GFP into the entorhinal cortices bilaterally."'
GSE14499_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"26 Samples total: 4 biological replicates of APP transgenic mice BDNF treated, 4 biological replicates of APP transgenic mice GFP treated, 3 biological replicates of non-trangenic mice sham lesion and 2 biological replicates of non-transgenic mice GFP treated for both tissues: Entorhinal cortex and hippocampus."'
GSE14525_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Acute lung injury (ALI), a major cause of acute respiratory failure with high morbidity and mortality, isare characterized by significant pulmonary inflammation and both alveolar and vascular barriers dysfunction.  In Pprior studies have highlighted the role of nonmuscle myosin light chain kinase (nmMLCK) as an essential element of inflammatory response with MYLK polymorphisms associated withwhich alters ALI susceptibility. In the present study we sought to further define nmMLCK in acute inflammatory syndromes and examined We examined nmMLCK as a molecular target involved in increase of lung epithelial and endothelial barrier permeability. We utilized in two muirine models of inflammatory lung injury: intratracheal administration of endotoxin/lipopolysaccharide (LPS, 2.5 mg/kg) and VILI (ventilator-induced lung injury, tidal volume 40ml/kg).  Two complementary strategies were used to reduce nmMLCK activity or expression. We found that membrane permeant oligopeptide, PIK, inhibited MLC kinase activity in vitro in aand displayed dose-dependent mannerinhibition of MLC kinase activity.. Intravenous delivery of PIK significantly attenuated LPS-induced lung inflammation reflected by decreasing accumulation of bronchoalveolar lavage (BAL) albumin (~ 50% reduction) as well as reduction in BAL cells, tissue MPO activity and tissue albumin in lung homogenates. A second regulatory approach explored targeting murine nmMLCK by administration of siRNA (5mg/kg) 3 days prior to LPS challenge. siRNA decreased of nmMLCK expression in lungs (~ 70% reduction) and resulted in significant attenuation LPS-induced lung inflammation (~ 40% reduction) as reflected by decreased BAL protein level and BAL cells. For targeting pulmonary vessels nmMLCK we used ACE antibody-conjugated liposomes with nmMLCK siRNA in murine ventilator-induced lung injury (VILI) model. Protein silencing of nmMLCK was evident by immunohistochemical analysis with a decrease in relative intensity of fluorescence in lung vessels compared with control animals. Furthermore, the inhibition of nmMLCK expression by siRNA in vessels significantly attenuated VILI lung injury as reflected by decreased BAL protein level (40% reduction). Finally, MLCK knockout mice were significantly protected (reduced BAL protein and albumin) when exposed to a model of severe VILI (4h, 40ml/kg tidal volume). Conclusion: the MLCK gene KO and chemical biology results indicate that the targeting of nmMLCK in vivo attenuate the severity of LPS-induced or VILI acute lung injury."'
GSE14525_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We used microarrays to detail the global programme of gene expression induced by VILI in Wild type and nmMLCK-/- mouse."'
GSE14525_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"four group (n=3) of animals were treated by SB (Spontaneouse breathing) or VILI (4 hours, 30 ml/kg tidal volume) in Wild type or nmMLCK-/- animals;"'
GSE14534_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Here we have used targeted RNA interference to suppress the expression of a number of key genes associated with IFN signalling in murine macrophages prior to activation. Genome-wide changes in transcript abundance caused by siRNA activity were measured using Affymetrix exon-arrays in the presence or absence of IFNγ stimulation. Transfection of murine bone-marrow derived macrophages (BMDMs) with non-targeting (control) siRNA and 11 sequence-specific siRNAs was performed using a cationic lipid transfection reagent (Lipofectamine2000) prior to stimulation with IFNγ. The 11 genes targeted were Ifnb1, Irf3, Stat1, Stat2, Nkfb2, Irf5, Casp4, Ifi47, Lyn, Sod2, and Traf1. Total RNA was harvested from cells and gene expression measured on Affymetrix GeneChip Mouse Exon 1.0 ST Arrays. "'
GSE14534_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"2. siRNA targeting experiments: 72 arrays in 12 different siRNA treatment groups, with each treatment group containing 6 arrays (3 replicates unstimulated, 3 replicates stimulated with IFNg). In each group a different targeting siRNA was used and in one group control non-targeting siRNA (RiscFree siRNA ThermoFisher) was used."'
GSE14539_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_title	"Chronic liver inflammation-induced double strand DNA breaks enhance hepatocarcinogenesis"'
GSE14539_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Surgical resection is the preferred treatment for Hepatocellular carcinoma; however, it induces tumor recurrence. Our objective was to understand the molecular mechanisms linking liver regeneration under chronic-inflammation to tumorigenesis. Mdr2-knockout mice, a model of inflammation-associated cancer, underwent partial-hepatectomy which led to enhanced hepatocarcinogenesis. Yet, liver regeneration in these mice was severely attenuated. We demonstrate the activation of the DNA damage response machinery and altered genomic instability during early liver inflammatory stages resulting in hepatocyte apoptosis and cell-cycle arrest, and suggest their involvement in tumor recurrence subsequent to partial hepatectomy. We propose that under the regenerative proliferative stress induced by liver resection, the genomic unstable hepatocytes generated during chronic-inflammation, escape apoptosis and reenter the cell-cycle, triggering the enhanced tumorigenesis"'
GSE14539_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Surgical resection is the preferred treatment for Hepatocellular carcinoma; however, it induces tumor recurrence. Our objective was to understand the molecular mechanisms linking liver regeneration under chronic-inflammation to tumorigenesis. Mdr2-knockout mice, a model of inflammation-associated cancer, underwent partial-hepatectomy which led to enhanced hepatocarcinogenesis. Yet, liver regeneration in these mice was severely attenuated. We demonstrate the activation of the DNA damage response machinery and altered genomic instability during early liver inflammatory stages resulting in hepatocyte apoptosis and cell-cycle arrest, and suggest their involvement in tumor recurrence subsequent to partial hepatectomy. We propose that under the regenerative proliferative stress induced by liver resection, the genomic unstable hepatocytes generated during chronic-inflammation, escape apoptosis and reenter the cell-cycle, triggering the enhanced tumorigenesis"'
GSE14549_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Gene expression profiling in liver of mice with a mutant Wrn protein treated with/without vitamin C compared to WT mice."'
GSE14549_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Microarray analyses were performed on the liver tissues of 9 months old mice. Four independent biological replicates of this experiment (wild type vs Wrn mutant or wild type vs vitamin C treated mutant mice) were carried out with a dye swap on two replicates of each genotype."'
GSE14550_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin (human array)"'
GSE14550_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify molecular mediators of podoplanin-induced effects we compared transcriptional profiles of podoplanin-overexpressing and control tumors."'
GSE14550_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify molecular mediators of podoplanin-induced effects we compared transcriptional profiles of podoplanin-overexpressing and control tumors."'
GSE14550_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_overall_design	"MCF7 human breast carcinoma cells were stably transfected with the pTet-Off-regulator plasmid and the pTRE2hyg response plasmid, comprising or not full-length cDNA of human podoplanin (transcript variant 1, GenBank Accession number NM_006474). Three podoplanin-overexpressing and three control clones were isolated and each of them was injected bilaterally into the mammary fat pads of five female nude mice. Tumors were harvested after 24 days of growth and RNA was extracted from each of them. RNA of the 10 tumors derived from the same cell clone was pooled to give a total of six samples for microarray analysis (3x podoplanin-overexpressing, 3x control)."'
GSE14551_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Gene expression profiling of tumor stroma of MCF7 breast cancer xenografts overexpressing podoplanin (mouse array)"'
GSE14551_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify potential molecular mediators of podoplanin-induced effects in the murine tumor stroma we compared transcriptional profiles of podoplanin-overexpressing and control tumors using mouse microarrays."'
GSE14551_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_summary	"Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify potential molecular mediators of podoplanin-induced effects in the murine tumor stroma we compared transcriptional profiles of podoplanin-overexpressing and control tumors using mouse microarrays."'
GSE14551_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_overall_design	"MCF7 human breast carcinoma cells were stably transfected with the pTet-Off-regulator plasmid and the pTRE2hyg response plasmid, comprising or not full-length cDNA of human podoplanin (transcript variant 1, GenBank Accession number NM_006474). Three podoplanin-overexpressing and three control clones were isolated and each of them was injected bilaterally into the mammary fat pads of five female nude mice. Tumors were harvested after 24 days of growth and RNA was extracted from each of them. RNA of the 10 tumors derived from the same cell clone was pooled to give a total of six samples for microarray analysis (3x podoplanin-overexpressing, 3x control)."'
GSE14552-GPL2986_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin"'
GSE14552-GPL2995_series_matrix.txtimp_info.txt	Found 'overexpressing' in '!Series_title	"Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin"'
GSE14559_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"To decipher the structure and behaviors of the transcription factor (TF) network, we created 50 permanent mouse ES cell lines, in each of which one of the 50 transcription factors tagged with FLAG, is inserted into the doxycycline (dox)-repressible ROSA26 locus. Expression profiling reveals Cdx2 as the most potent inducer of transcriptome perturbation in ES cells, followed by Esx1, Sox9, Tcf3, Klf4, and Gata3. Immunoprecipitation (IP) with a FLAG-antibody in Cdx2-induced ES cells, identifies NuRD in CDX2-associated protein complexes; and chromatin-IP-sequencing identifies CDX2-binding sites predominantly in genes up-regulated by CDX2. Compendium analyses of Cdx2- and the other TF-inducible ES cells suggest a central role of the POU5F1/SOX2/NANOG protein complex in a swift-acting control mechanism to down-regulate a common set of genes at the beginning of multi-lineage ES cell differentiations. These ES cell lines will be a valuable resource to study biological networks in ES cells and mice."'
GSE14586_series_matrix.txtimp_info.txt	Found 'overexpression' in '!Series_summary	"(F) Potential CDX2-direct target genes based on ChIP-Seq and the alteration of expression by Cdx2-overexpression."'
GSE14612_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"IFNg is a pro-inflammatory and pro-atherogenic cytokine that leads to macrophage activation. Adenosine has well-documented anti-inflammatory properties. We used microarrays to compare the global gene expression profile in mouse macrophages stimulated with IFNg alone and those cells treated with IFNg and adenosine."'
GSE14612_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"IFNg is a pro-inflammatory and pro-atherogenic cytokine that leads to macrophage activation. Adenosine has well-documented anti-inflammatory properties. We used microarrays to compare the global gene expression profile in mouse macrophages stimulated with IFNg alone and those cells treated with IFNg and adenosine."'
GSE14612_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"IFNg is a pro-inflammatory and pro-atherogenic cytokine that leads to macrophage activation. Adenosine has well-documented anti-inflammatory properties. We used microarrays to compare the global gene expression profile in mouse macrophages stimulated with IFNg alone and those cells treated with IFNg and adenosine."'
GSE14612_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"RAW 264.7 cells were treated for 4 hours with either IFNg or IFNg plus adenosine. Following treatment, total RNA was extracted and treatment groups were pooled from 2 separate experiments for hybridization of Affymetrix microarrays."'
GSE14629_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Phthalates are industrial additives widely used as plasticizers. In addition to deleterious effects on male genital development, population studies have documented correlations between phthalates exposure and impacts on reproductive tract development and on the metabolic syndrome in male adults. In this study we investigated potential mechanisms underlying the impact of di-(2-ethylhexyl)-phthalate (DEHP) on adult mouse liver in vivo. A parallel analysis of hepatic transcript and metabolic profiles from adult mice exposed to varying DEHP doses was performed. Hepatic genes modulated by DEHP are predominantly PPARα targets. However, the induction of prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways, including Constitutive Androstane Receptor (CAR). Integration of transcriptomic and metabonomic profiles revealed a correlation between the impacts of DEHP on genes and metabolites related to heme synthesis and on the Rev-erbα pathway that senses endogenous heme level."'
GSE14629_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Phthalates are industrial additives widely used as plasticizers. In addition to deleterious effects on male genital development, population studies have documented correlations between phthalates exposure and impacts on reproductive tract development and on the metabolic syndrome in male adults. In this study we investigated potential mechanisms underlying the impact of di-(2-ethylhexyl)-phthalate (DEHP) on adult mouse liver in vivo. A parallel analysis of hepatic transcript and metabolic profiles from adult mice exposed to varying DEHP doses was performed. Hepatic genes modulated by DEHP are predominantly PPARα targets. However, the induction of prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways, including Constitutive Androstane Receptor (CAR). Integration of transcriptomic and metabonomic profiles revealed a correlation between the impacts of DEHP on genes and metabolites related to heme synthesis and on the Rev-erbα pathway that senses endogenous heme level."'
GSE14629_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"One-color macroarrays, 4 experimental conditions: Control mice (vehicle treated), mice treated with di-(2-ethylhexyl)-phthalate (DEHP) at 30 mg/kg/day (D30), 180 mg/kg/day (D180) or 1100 mg/kg/day (D1100) for 14 days, Biological replicates: 6 controls, 4 D30, 4 D180, 5 D1100, One replicate per array"'
GSE14644_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"IL-4 induced gene expression was investigated in mouse bone marrow macrophages (BMM) of C57BL6/J and Balb/cAnNCrl mice. Differentiated BMM were incubated with mouse recombinant IL-4 for 4 or 18 hours or without for 18 hours. Two independent experiments were performed at each time (mock, 4 and 18 hours) using different mice littermates for each experiment."'
GSE14654_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"To study the function of Paf1C in mouse ESCs, we generated an ES cell line stably expressing a location and affinity purification (LAP)-tagged Ctr9 fusiuon protein using the bacterial astificial chromosome (BAC)-based TransgeneOmics approach. To investigate whether pluripotency and lineage control genes differentially regulated upon Paf1C depletion are direct targets of the Paf1C, we analyzed the binding of the Ctr9-LAP fusion protein by ChIP-chip and identified 2175 promoter regions that were bound by Ctr9."'
GSE14672_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"GM-CSF controls the development of granulocytes but little is known about the contribution of the downstream mediating transcription factor STAT5A/B.  To elucidate this pathway, we generated mice lacking the Stat5a and 5b genes in blood cells.  Peripheral neutrophils were decreased and administration of 5-FU and GM-CSF failed to induce granulopoiesis in Stat5a/b-mutant mice. GMPs were isolated and cultured with GM-CSF.  Both the number and size of STAT5A/B-null colonies were reduced and GM-CSF-induced survival of mature STAT5A/B-null neutrophils was impaired.  Time-lapse cinematography and single cell tracking of GMPs revealed that STAT5A/B-null cells were characterized by a longer generation time and an increased cell death.  Gene expression profiling experiments suggested that STAT5A/B directs GM-CSF signaling through the regulation of cell survival genes."'
GSE14672_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Mice lacking or with  the Stat5a and 5b genes in blood cells, which were treated w/o GMP"'
GSE14674_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Dendritic cell activation through ligation of pattern recognition receptors leading to full functional maturation causes induction of CD8 T cell immunity instead of tolerance through increased delivery of co-stimulatory signals. Here we investigate whether a prototypic organ-resident antigen-presenting cells, i.e. liver sinusoidal endothelial cells (LSEC), also switch from tolerogenic to immunogenic CD8 T cell activation upon such activation. We demonstrate by gene expression analysis that LSEC expressed numerous pattern recognition receptors that attributed sentinel function, but ligand-induced activation of these receptors was not sufficient to overcome tolerance induction of CD8 T cells. However, viral infection caused functional maturation of antigen-presenting LSEC and was sufficient to promote antigen-specific differentiation into fully functional effector CD8 T cells in the absence of dendritic cells. Thus, we identify a novel principle of inducing CD8 T cell immunity by virally infected organ-resident antigen-presenting cells employing distinct mechanisms compared to dendritic cells."'
GSE14674_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Dendritic cell activation through ligation of pattern recognition receptors leading to full functional maturation causes induction of CD8 T cell immunity instead of tolerance through increased delivery of co-stimulatory signals. Here we investigate whether a prototypic organ-resident antigen-presenting cells, i.e. liver sinusoidal endothelial cells (LSEC), also switch from tolerogenic to immunogenic CD8 T cell activation upon such activation. We demonstrate by gene expression analysis that LSEC expressed numerous pattern recognition receptors that attributed sentinel function, but ligand-induced activation of these receptors was not sufficient to overcome tolerance induction of CD8 T cells. However, viral infection caused functional maturation of antigen-presenting LSEC and was sufficient to promote antigen-specific differentiation into fully functional effector CD8 T cells in the absence of dendritic cells. Thus, we identify a novel principle of inducing CD8 T cell immunity by virally infected organ-resident antigen-presenting cells employing distinct mechanisms compared to dendritic cells."'
GSE14674_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Transcriptional profiles of untreated liver sinusoidal endothelial cells (LSEC) and LSEC, stimulated with either LPS (100ng/ml) or infected with MCMV-GFP (MOI=0.1) were compared on Illumina Mouse WG-6 BeadChip microarray platform. All samples represent biological replicates and were processed separately throughout the experiment. "'
GSE14691-GPL1261_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Myotonic dystrophy type 1 (DM1) is an RNA dominant disease in which mutant transcripts containing an expanded CUG repeat (CUGexp) cause muscle dysfunction by interfering with biogenesis of other mRNAs. The toxic effects of mutant RNA are mediated partly through sequestration of splicing regulator Muscleblind-like 1 (Mbnl1), a protein that binds to CUGexp RNA. A gene that is prominently affected encodes chloride channel 1 (Clcn1), resulting in hyperexcitability of muscle (myotonia). To identify DM1-affected genes and study mechanisms for dysregulation, we performed global mRNA profiling in transgenic mice that express CUGexp RNA, as compared to Mbnl1 knockout and Clcn1 null mice. We found that the majority of changes induced by CUGexp RNA in skeletal muscle can be explained by reduced activity of Mbnl1, including many changes that are secondary to myotonia. The pathway most affected comprises genes involved in calcium signaling and homeostasis. Some effects of CUGexp RNA on gene expression are caused by abnormal alternative splicing or downregulation of Mbnl1-interacting mRNAs. However, several of the most highly dysregulated genes showed altered transcription, as indicated by parallel changes of the corresponding premRNAs. These results support the idea that trans-dominant effects of CUGexp RNA on gene expression in this transgenic model may occur at the level of transcription, RNA processing, and mRNA decay, and are mediated mainly but not entirely through sequestration of Mbnl1."'
GSE14691-GPL339_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Myotonic dystrophy type 1 (DM1) is an RNA dominant disease in which mutant transcripts containing an expanded CUG repeat (CUGexp) cause muscle dysfunction by interfering with biogenesis of other mRNAs. The toxic effects of mutant RNA are mediated partly through sequestration of splicing regulator Muscleblind-like 1 (Mbnl1), a protein that binds to CUGexp RNA. A gene that is prominently affected encodes chloride channel 1 (Clcn1), resulting in hyperexcitability of muscle (myotonia). To identify DM1-affected genes and study mechanisms for dysregulation, we performed global mRNA profiling in transgenic mice that express CUGexp RNA, as compared to Mbnl1 knockout and Clcn1 null mice. We found that the majority of changes induced by CUGexp RNA in skeletal muscle can be explained by reduced activity of Mbnl1, including many changes that are secondary to myotonia. The pathway most affected comprises genes involved in calcium signaling and homeostasis. Some effects of CUGexp RNA on gene expression are caused by abnormal alternative splicing or downregulation of Mbnl1-interacting mRNAs. However, several of the most highly dysregulated genes showed altered transcription, as indicated by parallel changes of the corresponding premRNAs. These results support the idea that trans-dominant effects of CUGexp RNA on gene expression in this transgenic model may occur at the level of transcription, RNA processing, and mRNA decay, and are mediated mainly but not entirely through sequestration of Mbnl1."'
GSE14691-GPL340_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Myotonic dystrophy type 1 (DM1) is an RNA dominant disease in which mutant transcripts containing an expanded CUG repeat (CUGexp) cause muscle dysfunction by interfering with biogenesis of other mRNAs. The toxic effects of mutant RNA are mediated partly through sequestration of splicing regulator Muscleblind-like 1 (Mbnl1), a protein that binds to CUGexp RNA. A gene that is prominently affected encodes chloride channel 1 (Clcn1), resulting in hyperexcitability of muscle (myotonia). To identify DM1-affected genes and study mechanisms for dysregulation, we performed global mRNA profiling in transgenic mice that express CUGexp RNA, as compared to Mbnl1 knockout and Clcn1 null mice. We found that the majority of changes induced by CUGexp RNA in skeletal muscle can be explained by reduced activity of Mbnl1, including many changes that are secondary to myotonia. The pathway most affected comprises genes involved in calcium signaling and homeostasis. Some effects of CUGexp RNA on gene expression are caused by abnormal alternative splicing or downregulation of Mbnl1-interacting mRNAs. However, several of the most highly dysregulated genes showed altered transcription, as indicated by parallel changes of the corresponding premRNAs. These results support the idea that trans-dominant effects of CUGexp RNA on gene expression in this transgenic model may occur at the level of transcription, RNA processing, and mRNA decay, and are mediated mainly but not entirely through sequestration of Mbnl1."'
GSE14698_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_title	"Microarray Experiments for mice lacking or with  the Stat5a and 5b genes in blood cells that were treated w/o CMP"'
GSE14698_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Microarray Experiments for mice lacking or with  the Stat5a and 5b genes in blood cells that were treated w/o CMP"'
GSE14699_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Peripheral tolerance induction is critical for the maintenance of self-tolerance and can be mediated by immunoregulatory T cells or by direct induction of T cell anergy or deletion. While the molecular processes underlying anergy have been extensively studied, little is known about the molecular basis for peripheral T cell deletion. Here, we determined the gene expression signature of peripheral CD8+ T cells undergoing deletional tolerance, relative to those undergoing immunogenic priming or lymphopenia-induced proliferation. From these data, we report the first detailed molecular signature of cells undergoing deletion."'
GSE14699_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Naïve (CD44lo) OT-I T cells were CFSE labelled and transferred in a model of deletional tolerance (RIP-OVAhi mice), a model of immunity (mice primed with OVA coated splenocytes and LPS) or a model of lymphopenia induced proliferation (Rag-/- mice).  60 hrs (RIP-OVAhi and OVA coated splenocytes) or 5 days (Rag-/-) after transfer, OT-I cells that had undergone two or more divisions as determined by CFSE dilution were sorted, RNA extracted and samples were prepared for hybridisation to Affymetrix microarrays.  As a control for naive cells, CFSE labelled OT-I cells were injected into antigen-free B6 mice and the undivided naive cells were sorted after 60 hrs and also used for microarray analysis.  Two replicates were prepared for the naive cells, cells from RIP-OVAhi mice and cells from OVA coated splenocyte primed mice, while one replicate was prepared for the cells from Rag-/- mice."'
GSE14710_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_summary	"Keywords: stat5 KO or WT treated or w/o GH"'
GSE14710_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Total 6 WT controls and 6 stat5a/b KO mice, treated or w/o GH"'
GSE14715_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Mutations of MECP2 (Methyl-CpG Binding Protein 2) cause Rett Syndrome. As a chromatin associated multifunctional protein, how MeCP2 integrates external signals and regulates neuronal function remain unclear. While neuronal activity-induced phosphorylation of MeCP2 at serine 421 (S421) has been reported, the full spectrum of MeCP2 phosphorylation together with the in vivo function of such modifications are yet to be revealed. Here we report the identification of several novel MeCP2 phosphorylation sites in normal and epileptic brains from multiple species. We demonstrate that serine 80 (S80) phosphorylation of MeCP2 is critical as its mutation into alanine (S80A) in transgenic knock-in mice leads to locomotor deficits. S80A mutation attenuates MeCP2 chromatin association at several gene promoters in resting neurons and leads to transcription changes of a small number of genes. Calcium influx in neurons causes dephosphorylation at S80, potentially contributing to its dissociation from the chromatin. We postulate that phosphorylation of MeCP2 modulates its dynamic function in neurons transiting between resting and active states within neural circuits that underlie behaviors."'
GSE14715_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"E 15.5 Mecp2 -/y cortical neurons were infected with lentivirus expressing wild-type and S80A mutant MeCP2 at similar protein expression level. 2 biological independent samples and dye swap were used for this set (GSM367413) and replicate 2 set (GSM367414)."'
GSE14721_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Articular tissues of all mices were collected at the peak time of clinical severity (four weeks before booster),  for RNA extraction and hybridization on Affymetrix microarrays. We induces CIA with chicken collagen type II, emulsified with Complet Adjuvant of Freund, and the controls were mice induced only with Complet Adjuvant of Freund with or without MLIF"'
GSE14769_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The innate immune system is a two-edged sword; it is absolutely required for host defense against infection, but if left uncontrolled can trigger a plethora of inflammatory diseases.  Here we used systems biology approaches to predict and validate a gene regulatory network involving a dynamic interplay between the transcription factors NF-κB, C/EBPδ, and ATF3 that controls inflammatory responses.  We mathematically modeled transcriptional regulation of Il6 and Cebpd genes and experimentally validated the prediction that the combination of an initiator (NF-κB), an amplifier (C/EBPδ) and an attenuator (ATF3) forms a regulatory circuit that discriminates between transient and persistent Toll-like receptor 4-induced signals. Our results suggest a mechanism that enables the innate immune system to detect the duration of infection and to respond appropriately."'
GSE14769_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Bone marrow-derived macrophages stimulated with LPS for 0, 20, 40, 60, 80, 120, 240 and 360 minutes."'
GSE14774_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Environmental reproductive health focuses on the effect of exposure to contaminants considered as endocrine disruptors. Developmental testis is considered as target of these compounds affecting testicular functions in adults and suspected implications in tumor etiology. Comparative analysis of gene expression in mouse testis exposed to five disruptors, three different dosages and three accumulative developmental stages shown defined signature profiles of gene deregulation for MEHP (monoethyl phthalate) and zearalenone (a phytoestrogen) and different to 17β-estradiol exposure. The effects are even detected in postpuberal male offspring from premating exposed mothers. Oxidative stress response, protein ubiquitination and oxidative phosphorylation are the most representative pathways affected."'
GSE14774_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"	CD-1 mice were in vivo exposed to several doses of EDs following a defined protocol: mothers were exposed two weeks before mating (exposure A); the same exposure and dose were maintained during pregnancy (exposure B) and four weeks after birth (exposure C). In all exposures, male offspring were sacrificed to obtain the testes."'
GSE14810_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Fully differentiated 3T3 L1 and C3H/10T1/2 adipocytes were treated with RSG, or DMSO vehicle for 1, 2, 4, 7, 24, and 48 hrs, and total RNA was extracted for microarray analysis."'
GSE14812_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"Chromatin immunoprecipitation of C/EBP delta in mouse bone-marrow macrophages stimulated with LPS for 6hr"'
GSE14812_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"The innate immune system is a two-edged sword; it is absolutely required for host defense against infection, but if left uncontrolled can trigger a plethora of inflammatory diseases.  Here we used systems biology approaches to predict and validate a gene regulatory network involving a dynamic interplay between the transcription factors NF-kB, C/EBPd, and ATF3 that controls inflammatory responses.  We mathematically modeled transcriptional regulation of Il6 and Cebpd genes and experimentally validated the prediction that the combination of an initiator (NF-kB), an amplifier (C/EBPd) and an attenuator (ATF3) forms a regulatory circuit that discriminates between transient and persistent Toll-like receptor 4-induced signals. Our results suggest a mechanism that enables the innate immune system to detect the duration of infection and to respond appropriately."'
GSE14826_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_title	"A serine protease inhibitor induces necrosis of infected macrophages within granulomas during activation of tuberculosis"'
GSE14829_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The similarity of transcription profiles among serum-starved fibroblasts of all different WT and ras knockout genotypes tested, indicated that H-Ras and N-Ras do not play significant roles in control of transcriptional responses to serum deprivation stress. In contrast, genomic disruption of H-ras or N-ras, individually or in combination, determined highly specific, differential gene expression profiles in response to post-starvation stimulation with serum for 1 hour (G0/G1 transition) or for 8 hours (mid-G1 progression). The absence of N-Ras caused significantly higher changes than the absence of H-Ras on the wave of transcriptional activation linked to G0/G1 transition. In contrast, the absence of H-Ras affected more potently the profile of the transcriptional wave detected during mid-G1 progression. Functional analysis demonstrated a predominant functional association of H-Ras with growth and proliferation, whereas N-Ras exhibited a closer functional link to development or cell cycle regulation as well as immunomodulation and apoptosis. Mechanistic analysis indicated that ERK-dependent activation of Stat1 mediates the regulatory effect of N-Ras on defense and immunity, whereas the pro-apoptotic effects of N-Ras are mediated through ERK and p38 signaling.  Our observations support previous reports of an absolute requirement for different peaks of Ras activity during the initial stages of the cell cycle and confirm the notion of functional specificity for the H-Ras and N-Ras isoforms."'
GSE14829_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_overall_design	"Mus musculus cell lines from the appropriate ras genotype were harvested on Dulbecco’s modified Eagle’s medium (DMEM) supplemented with fetal bovine serum (10% FBS), glutamine (2mM), penicillin (100 U/ml) and streptomycin (100 mg/ml). Cultures were grown in a humidified CO2 (5%) atmosphere at 37°C and when subconfluent cells were starved for 24 hours. After starvation cells were either used for RNA isolation, or induced for 1 hour or 8 hours with 20% fetal bovine serum and then RNA extraction and isolation was carried out for hybridization on Affymetrix microarrays."'
GSE14843-GPL1261_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Methods and Results–Mice were divided into three treatment groups: sham-operation, ischemia-reperfusion (I/R), and myocardial infarction. Mice with liver I/R were included as additional controls. Marked changes in hepatic gene expression were observed after 24 hours, despite the lack of histological changes in the liver. Genes related to tissue remodeling, adhesion molecules, and morphogenesis were significantly upregulated in the livers of mice with myocardial I/R or infarction, but not in those with liver I/R. Myocardial ischemia, but not changes in the hemodynamic state, was postulated to significantly alter hepatic gene expression. Moreover, detailed analysis of the signaling pathway suggested the presence of humoral factors that intervened between the heart and liver. To address these points, we utilized isolated primary hepatocytes and showed that osteopontin released from the heart actually altered the signaling pathways of primary hepatocytes to those observed in the livers of mice under myocardial ischemia. Moreover, osteopontin stimulated primary hepatocytes to secrete vascular endothelial growth factor-A, which is important for tissue remodeling."'
GSE14843-GPL1261_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"C57BL/6J mice (n=46, BW 24.1±1.42 g, 8–10 weeks of age; Charles River Laboratories) were divided into the following treatment groups: sham-operated (n=11), I/R (n=10), myocardial infarction (n=10), liver I/R (n=10), and sham-operated plus hydralazine (n=5). In this study, we examined the response of hepatic gene expression to myocardial ischemia. Given the systemic inflammation that characterizes acute coronary syndromes, we postulated that regulation of hepatic genes occurs via inflammatory mediators and not via alterations in hemodynamics or hepatic perfusion. We therefore used whole genome transcriptional profiling to identify hepatic genes selectively regulated in the setting of myocardial ischemia. Moreover, detailed analysis of the signaling pathway suggested the presence of humoral factors that intervened between the heart and liver under myocardial ischemia. As a candidate humoral factors, osteopontin was further investigated. To evaluate whether the cardiac secreted protein affects hepatic gene expressions, we investigated primary hepatocytes treated with osteopontin by using microarray analysis. Affymetrix GeneChip Mouse Genome 430 2.0 Array was used to measure gene expression levels in primary hepatocytes at 8 hours after osteopontin stimulation (mock: n=3 and osteopontin: n=3)."'
GSE14843-GPL8224_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_summary	"Methods and Results–Mice were divided into three treatment groups: sham-operation, ischemia-reperfusion (I/R), and myocardial infarction. Mice with liver I/R were included as additional controls. Marked changes in hepatic gene expression were observed after 24 hours, despite the lack of histological changes in the liver. Genes related to tissue remodeling, adhesion molecules, and morphogenesis were significantly upregulated in the livers of mice with myocardial I/R or infarction, but not in those with liver I/R. Myocardial ischemia, but not changes in the hemodynamic state, was postulated to significantly alter hepatic gene expression. Moreover, detailed analysis of the signaling pathway suggested the presence of humoral factors that intervened between the heart and liver. To address these points, we utilized isolated primary hepatocytes and showed that osteopontin released from the heart actually altered the signaling pathways of primary hepatocytes to those observed in the livers of mice under myocardial ischemia. Moreover, osteopontin stimulated primary hepatocytes to secrete vascular endothelial growth factor-A, which is important for tissue remodeling."'
GSE14843-GPL8224_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"C57BL/6J mice (n=46, BW 24.1±1.42 g, 8–10 weeks of age; Charles River Laboratories) were divided into the following treatment groups: sham-operated (n=11), I/R (n=10), myocardial infarction (n=10), liver I/R (n=10), and sham-operated plus hydralazine (n=5). In this study, we examined the response of hepatic gene expression to myocardial ischemia. Given the systemic inflammation that characterizes acute coronary syndromes, we postulated that regulation of hepatic genes occurs via inflammatory mediators and not via alterations in hemodynamics or hepatic perfusion. We therefore used whole genome transcriptional profiling to identify hepatic genes selectively regulated in the setting of myocardial ischemia. Moreover, detailed analysis of the signaling pathway suggested the presence of humoral factors that intervened between the heart and liver under myocardial ischemia. As a candidate humoral factors, osteopontin was further investigated. To evaluate whether the cardiac secreted protein affects hepatic gene expressions, we investigated primary hepatocytes treated with osteopontin by using microarray analysis. Affymetrix GeneChip Mouse Genome 430 2.0 Array was used to measure gene expression levels in primary hepatocytes at 8 hours after osteopontin stimulation (mock: n=3 and osteopontin: n=3)."'
GSE14862_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Intestinal ischemia-reperfusion (IR) injury is initiated when natural IgM antibodies recognize neo-epitopes that are revealed on ischemic cells. The target molecules and mechanisms whereby these neo-epitopes become accessible to recognition are not well understood. Proposing that isolated intestinal epithelial cells (IEC) may carry IR-related neo-epitopes, we used in vitro IEC binding assays to screen hybridomas created from B cells of unmanipulated wild type C57BL/6 mice. We identified a novel IgM monoclonal antibody (mAb B4) that reacted with the surface of IEC by flow cytometric analysis and was alone capable of causing complement activation, neutrophil recruitment and intestinal injury in otherwise IR-resistant Rag1-/- mice. Monoclonal Ab B4 was found to specifically recognize mouse annexin IV. Pre-injection of recombinant annexin IV blocked IR injury in wild type C57BL/6 mice, demonstrating the requirement for recognition of this protein in order to develop IR injury in the context of a complex natural antibody repertoire. Humans were also found to exhibit IgM natural antibodies that recognize annexin IV. These data in toto identify annexin IV as a key ischemia-related target antigen that is recognized by natural Abs in a pathologic process required in vivo to develop intestinal IR injury."'
GSE14869_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"The nuclear receptor peroxisome proliferator-activated receptor alpha (PPARα) regulates responses to chemical or physical stress in part by altering expression of genes involved in proteome maintenance.  Many of these genes are also transcriptionally regulated by heat shock (HS) through activation by HS factor-1 (HSF1).  We hypothesized that there are interactions on a genetic level between PPARα and the HS response mediated by HSF1.  Wild-type and PPARα-null mice were exposed to HS, the PPARα agonist WY-14,643 (WY), or both; gene and protein expression was examined in the livers of the mice 4 or 24 hrs after HS.  Gene expression profiling identified a number of Hsp family members that were altered similarly in both mouse strains.  However, most of the targets of HS did not overlap between strains.  A subset of genes was shown by microarray and RT-PCR to be regulated by HS in a PPARα-dependent manner.  HS also down-regulated a large set of mitochondrial genes specifically in PPARα-null mice that are known targets of PPARg co-activator 1 (PGC-1) family members.  Pretreatment of PPARα-null mice with WY increased expression of PGC-1b and target genes and prevented the down-regulation of the mitochondrial genes by HS.  A comparison of HS genes regulated in our dataset with those identified in wild-type and HSF1-null mouse embryonic fibroblasts indicated that although many HS genes are regulated independently of both PPARα and HSF1, a number require both factors for HS responsiveness.  These findings demonstrate that the PPARα genotype has a dramatic effect on the transcriptional targets of HS and support an expanded role for PPARα in the regulation of proteome maintenance genes after exposure to diverse forms of environmental stress including HS."'
GSE14869_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"The nuclear receptor peroxisome proliferator-activated receptor alpha (PPARα) regulates responses to chemical or physical stress in part by altering expression of genes involved in proteome maintenance.  Many of these genes are also transcriptionally regulated by heat shock (HS) through activation by HS factor-1 (HSF1).  We hypothesized that there are interactions on a genetic level between PPARα and the HS response mediated by HSF1.  Wild-type and PPARα-null mice were exposed to HS, the PPARα agonist WY-14,643 (WY), or both; gene and protein expression was examined in the livers of the mice 4 or 24 hrs after HS.  Gene expression profiling identified a number of Hsp family members that were altered similarly in both mouse strains.  However, most of the targets of HS did not overlap between strains.  A subset of genes was shown by microarray and RT-PCR to be regulated by HS in a PPARα-dependent manner.  HS also down-regulated a large set of mitochondrial genes specifically in PPARα-null mice that are known targets of PPARg co-activator 1 (PGC-1) family members.  Pretreatment of PPARα-null mice with WY increased expression of PGC-1b and target genes and prevented the down-regulation of the mitochondrial genes by HS.  A comparison of HS genes regulated in our dataset with those identified in wild-type and HSF1-null mouse embryonic fibroblasts indicated that although many HS genes are regulated independently of both PPARα and HSF1, a number require both factors for HS responsiveness.  These findings demonstrate that the PPARα genotype has a dramatic effect on the transcriptional targets of HS and support an expanded role for PPARα in the regulation of proteome maintenance genes after exposure to diverse forms of environmental stress including HS."'
GSE14869_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"total 24 samples, 3 per group, for controls and treated."'
GSE14890_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"Expression data of LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- mice."'
GSE14890_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."'
GSE14891_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_title	"Expression data of LPS-stimulated macrophages from wild-type and Zc3h12a-/- mice."'
GSE14891_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Peritoneal macrophages from wild-type and Zc3h12a-/- mice were stimulated with LPS for 0, 1, 2 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."'
GSE14898_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Aortic endothelia from mice exposed to dietary model of type II diabetes at 4, 6 and 8 weeks of exposure to Bio-Serv #S3282 diet.  Objective: Type II diabetes is associated with endothelial dysfunction, which can contribute to accelerated atherosclerosis and subsequent cardiovascular events. We seek to identify transcripts dysregulated in vivo in response to chronic exposure to high dietary fat that leads to diabetes.  "'
GSE14898_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_summary	"Methods: Beginning at 8 weeks of age, male Tie2-GFP mice (transgenically expressing green fluorescent protein exclusively within the endothelia) were fed a 60% fat calorie diet (Bio-Serv #S3282); age-matched mice were fed normal chow. After 4, 6, and 8 weeks on the diet, aortae and skeletal muscles (gastrocnemius, biceps femoris, and plantaris) were excised, minced, and collagenolytically digested. Each tissue digest was then subjected to FACS in order to obtain 10,000 endothelial cells. Transcriptomic analyses were performed with microarrays containing the Operon Murine V4 oligo set, and highly dysregulated genes were confirmed by real-time PCR. Results: By 4 weeks, Tie2-GFP mice receiving a high fat diet exhibited a fasting glucose of 215+17 mg/dL vs. 134+23 mg/dL in controls; by 6 weeks, a high fat diet resulted in lower glucose tolerance vs. control diet. Following 4, 6, and 8 weeks of high-fat regimen, aortic endothelial transcripts up-regulated by greater than 2-fold in biologically replicate experiments included macrophage inflammatory protein 2 (Mip2), chemokine (C-C motif) ligand 9 (CCL9), galectin-3 (Gal-3), and 5-lipoxygenase-activating protein (FLAP). Endothelial transcripts up-regulated in skeletal muscle included Mip2, CCL8 and 9, FLAP, gal-1 and 3, and ferritin light chain 1 (FTL1); transcripts down-regulated in muscle included endothelin-1 (ET-1) and insulin-like growth factor II (IGF II). Discussion: Gal-3 and FTL-1 are known to increase in response to advanced glycation end-products and oxidized LDL, respectively. However, the down-regulation of ET-1 and IGFII was surprising, as the transcription of these genes has previously been thought to exacerbate atherosclerosis. In conclusion, a comprehensive analysis of the endothelial transcript-level response to a dietary model of Type II diabetes has revealed novel regulation of transcripts with roles in inflammation, insulin sensitivity, oxidative stress, and atherosclerosis. Understanding the mechanism of diabetes-associated endothelial dysfunction may lead to improved therapies that lower the risk of cardiovascular complications in diabetic patients. "'
GSE14917_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"We have previously demonstrated that deletion of the Cebpa gene in the developing fetal mouse lung caused death soon after birth from the failure of lung maturation.  Many of the transcriptional pathways regulating morphogenesis of the fetal lung are induced postnatally and mediate repair of the injured lung.  We hypothesized that C/EBPa plays a role in protection of the alveolar epithelium following hyperoxia injury of the mature lung.  Transgenic Cebpa∆/∆ mice in which Cebpa was conditionally deleted from Clara cells (from early gestation) and type II cells (from near-term) were developed.  Cebpa∆/∆ mice grow normally without any pulmonary abnormalities. Cebpa∆/∆ mice were highly susceptible to hyperoxia. Cebpa∆/∆ mice died within 4d after hyperoxia associated with severe lung inflammation and altered surfactant components at a time when all control mice survived.  Microarrays were analyzed on isolated type II cells at an early stage (24h) of hyperoxia exposure to detect the primary genes influenced by deletion of Cebpa.  The associated network analysis revealed the reduced expression of key genes related to surfactant lipid and protein homeostasis, such as Srebf, Scap, Lpcat1, Abca3, Sftpb, and Napsa.  Genes for the cell signaling, immune response, and protective antioxidants, including GSH and Vnn-1,3, were decreased in the Cebpa∆/∆ mice lung.  C/EBPa did not play a critical role in postnatal pulmonary function under normal conditions.  In contrast, in the absence of C/EBPa, exposure to hyperoxia caused respiratory failure, supporting the concept that C/EBPa plays an important role in enhancing epithelial cell survival, surfactant lipid homeostasis, and maturation of SP-B from pro-SP-B. "'
GSE14917_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"We have previously demonstrated that deletion of the Cebpa gene in the developing fetal mouse lung caused death soon after birth from the failure of lung maturation.  Many of the transcriptional pathways regulating morphogenesis of the fetal lung are induced postnatally and mediate repair of the injured lung.  We hypothesized that C/EBPa plays a role in protection of the alveolar epithelium following hyperoxia injury of the mature lung.  Transgenic Cebpa∆/∆ mice in which Cebpa was conditionally deleted from Clara cells (from early gestation) and type II cells (from near-term) were developed.  Cebpa∆/∆ mice grow normally without any pulmonary abnormalities. Cebpa∆/∆ mice were highly susceptible to hyperoxia. Cebpa∆/∆ mice died within 4d after hyperoxia associated with severe lung inflammation and altered surfactant components at a time when all control mice survived.  Microarrays were analyzed on isolated type II cells at an early stage (24h) of hyperoxia exposure to detect the primary genes influenced by deletion of Cebpa.  The associated network analysis revealed the reduced expression of key genes related to surfactant lipid and protein homeostasis, such as Srebf, Scap, Lpcat1, Abca3, Sftpb, and Napsa.  Genes for the cell signaling, immune response, and protective antioxidants, including GSH and Vnn-1,3, were decreased in the Cebpa∆/∆ mice lung.  C/EBPa did not play a critical role in postnatal pulmonary function under normal conditions.  In contrast, in the absence of C/EBPa, exposure to hyperoxia caused respiratory failure, supporting the concept that C/EBPa plays an important role in enhancing epithelial cell survival, surfactant lipid homeostasis, and maturation of SP-B from pro-SP-B. "'
GSE14917_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_overall_design	"Transgenic Cebpa delta/delta mice in which Cebpa was conditionally deleted from Clara cells (from early gestation) and type II cells (from near-term) were developed. Microarrays were analyzed on isolated type II cells at an early stage (0h, 2h, 24h) of hyperoxia exposure to detect the primary genes influenced by deletion of Cebpa."'
GSE14920_series_matrix.txtimp_info.txt	Found 'activation' in '!Series_summary	"Di-(2-ethylhexyl)-phthalate (DEHP), a widely used plasticizer, is detected in consumer’s body fluids. Contamination occurs through environmental and food chain sources. In mouse liver, DEHP activates the peroxisome proliferator-activated receptor alpha (PPARalpha) and regulates the expression of its target genes. Several in vitro investigations support the simultaneous recruitment of additional nuclear receptor pathways.  We investigated, in vivo, the hepatic impact of low doses of DEHP on PPARalpha activation, and the putative activation of additional signalling pathways. Wild-type and PPARalpha-deficient mice were exposed to different doses of DEHP. Gene expression profiling delineated the role of PPARalpha and revealed a PPARalpha-independent regulation of several prototypic Constitutive Androstane Receptor (CAR) target genes.   This finding demonstrates that CAR also represents a transcriptional regulator sensitive to phthalates. CAR-mediated effects of DEHP provide a new rationale for most endpoints of phthalates toxicity described previously, including endocrine disruption, hepatocarcinogenesis and the metabolic syndrome."'
GSE14920_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"One-color macroarrays, 6 experimental conditions: Wild type (WT) and PPARalpha-deficient mice (PPAR) were treated with vehicle (Ctrl) or with di-(2-ethylhexyl)-phthalate (DEHP) at 20 mg/kg/day (D20) or 200 mg/kg/day (D200) for 21 days, Biological replicates: 10 for each group, One replicate per array"'
GSE14937_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Experimental design:    The ovarian cycles of 90- and 180-day old mice with the lethal yellow mutation in the agouti gene (C57BL/6J Ay/a) and their non-mutated black littermates (C57BL6 a/a) (n=3 per group) were synchronized with the GnRH antagonist, Antide.  At 36 hours after the Antide injections, the mice were stimulated to ovulate with an injection of eCG.  At 36 hours after eCG injection the mice were euthanized and the ovaries collected.  One ovary from each animal was preserved in RNAlater for DNA microarray analysis."'
GSE14937_series_matrix.txtimp_info.txt	Found 'stimulated' in '!Series_overall_design	"Manipulations of biological samples and protocols used:  The ovarian cycles of 90- and 180-day old mice with the lethal yellow mutation in the agouti gene (C57BL/6J Ay/a) and their non-mutated black littermates (C57BL6 a/a) (n=3 per group) were synchronized with the GnRH antagonist, Antide.  At 36 hours after the Antide injections, the mice were stimulated to ovulate with an injection of eCG.  At 36 hours after eCG injection the mice were euthanized and the ovaries collected.  One ovary from each animal was preserved in RNAlater for DNA microarray analysis."'
GSE14937_series_matrix.txtimp_info.txt	Found 'treated' in '!Series_overall_design	"Technical protocols:  The ovaries were collected into RNAlater (Ambion) and stored at -80C until processed.  The RNAlater was blotted from the ovaries and each was individually homogenized in TRI reagent (MRC).  Bromochloropropane and sodium acetate were added, and the samples were centrifuged to separate the phases.  The RNA-containing layer was removed and the RNA purified on an RNeasy extraction column (Qiagen).  The sample was treated with an on-column DNase treatment (RNase-free DNase, Qiagen).  The purity and quantity were evaluated by an Agilent Bioanalyzer using the RNA 6000 Nanoassay LabChip."'
GSE14958_series_matrix.txtimp_info.txt	Found 'exposure' in '!Series_summary	"Natural antibodies, which arise without known immune exposure, have been described that specifically recognize cells dying from apoptosis but their role in innate immunity remains poorly understood. Herein, we show that the immune response to neo-antigenic determinants on apoptotic thymocytes is dominated by antibodies to oxidation-associated antigens, phosphorylcholine (PC), a head group that becomes exposed during programmed-cell death, and malondialdehyde (MDA), a reactive aldehyde degradation product of polyunsaturated lipids produced following exposure to reactive-oxidation species. While natural antibodies to apoptotic cells in naïve adult mice were dominated by PC and MDA specificities, the amounts of these antibodies were substantially boosted by treatment of mice with apoptotic cells. Moreover, the relative amounts of PC and MDA antibodies was affected by VH gene inheritance. Antibody interactions with apoptotic-cells also mediated the recruitment of C1q, which alone can promote apoptotic-cell phagocytosis by immature dendritic cells. Significantly, IgM-antibodies to both PC and MDA were primary factors in determining the efficiency of serum-dependent apoptotic-cell phagocytosis. Hence, we demonstrate a mechanism by which certain natural antibodies that recognize neo-antigens on apoptotic cells, in naïve mice and those induced by immune exposure to apoptotic-cells, can enhance the functional capabilities of immature dendritic cells for phagocytic engulfment of apoptotic cells."'
GSE14958_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Natural antibodies, which arise without known immune exposure, have been described that specifically recognize cells dying from apoptosis but their role in innate immunity remains poorly understood. Herein, we show that the immune response to neo-antigenic determinants on apoptotic thymocytes is dominated by antibodies to oxidation-associated antigens, phosphorylcholine (PC), a head group that becomes exposed during programmed-cell death, and malondialdehyde (MDA), a reactive aldehyde degradation product of polyunsaturated lipids produced following exposure to reactive-oxidation species. While natural antibodies to apoptotic cells in naïve adult mice were dominated by PC and MDA specificities, the amounts of these antibodies were substantially boosted by treatment of mice with apoptotic cells. Moreover, the relative amounts of PC and MDA antibodies was affected by VH gene inheritance. Antibody interactions with apoptotic-cells also mediated the recruitment of C1q, which alone can promote apoptotic-cell phagocytosis by immature dendritic cells. Significantly, IgM-antibodies to both PC and MDA were primary factors in determining the efficiency of serum-dependent apoptotic-cell phagocytosis. Hence, we demonstrate a mechanism by which certain natural antibodies that recognize neo-antigens on apoptotic cells, in naïve mice and those induced by immune exposure to apoptotic-cells, can enhance the functional capabilities of immature dendritic cells for phagocytic engulfment of apoptotic cells."'
GSE14969_series_matrix.txtimp_info.txt	Found 'induced' in '!Series_summary	"Although natural antibodies (NAbs) are present from birth, little is known about what drives their selection, and whether they have housekeeping functions. We now show that the prototypic T15-NAb, first identified because of its protective role in infection, is representative of a previously unknown type of NAb response that specifically recognizes and forms complexes with apoptotic cells, and which promotes cell-corpse engulfment by phagocytes. This T15-NAb-mediated process is dependent on the recruitment of C1q and mannose-binding lectin (MBL), which have known immune modulatory activities that also provide “eat me” signals for phagocytic clearance. Further investigation revealed that, the addition of T15-NAb significantly suppressed in vitro macrophage LPS-induced TNF-alpha and IL-6 secretion, as well as in vitro Toll-like receptor (TLR)-induced dendritic cell maturation and secretion of pro-inflammatory cytokines and chemokines. Significantly, high doses of this B-1 cell produced NAb also inhibited in vivo TLR–induced pro-inflammatory responses, and could suppress autoimmune inflammatory arthritis. These studies identify and characterize a previously unknown regulatory circuit by which a NAb product of innate-like B cells aids homeostasis by control of fundamental inflammatory pathways."'
GSE14980_series_matrix.txtimp_info.txt	Found 'expressing' in '!Series_overall_design	"Both vector control and GATA1-expressing cells were isolated by FACS for GFP and 18 and 42 hours.  Biologic triplicates were performed for each construct at each timepoint."'