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Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.
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View Samples3T3-L1 fibroblasts are a commonly used in vitro model for adipogenesis. When induced with hormones, they differentiate into mature fat cells. Here, microarrays were used to study 3T3-L1 adipose differentiation through time.
Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.
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View SamplesGene expression was studied from different mouse tissues
Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activity.
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View SamplesIron overload causes the generation of reactive oxygen species, which can lead to lasting damage to the liver and other organs. We studied the effects of iron deficiency and iron overload on the hepatic transcriptional and metabolomic profile in mouse models. Overall design: We studied effect of different iron overloads (High, medium and Low) on liver transcriptome using whole genome transcriptome profiling.
Nicotinamide N-methyltransferase expression decreases in iron overload, exacerbating toxicity in mouse hepatocytes.
Cell line, Subject
View SamplesIron overload causes the generation of reactive oxygen species, which can lead to lasting damage to the liver and other organs. We studied the effects of iron deficiency and iron overload on the hepatic transcriptional and metabolomic profile in mouse models. Overall design: We studied effect of different iron deficiency by HJV gene knockout mice on liver transcriptome using whole genome transcriptome profiling.
Nicotinamide N-methyltransferase expression decreases in iron overload, exacerbating toxicity in mouse hepatocytes.
Specimen part, Subject
View SamplesThe transcriptional profile of A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs) Overall design: A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs)
Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation.
Treatment, Subject
View SamplesThe transcriptional profile of A673 parental, and SP-2509 drug resistant washout cells (4 and 6 months) Overall design: Following generation of A673 SP-2509 drug resistant cells (chronic exposure for 7 months), drug was withdrawn with cell pellets collected 4 and 6 months after removal.
Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation.
Disease, Treatment, Subject
View SamplesIdentification of gene expressed in the enriched inner medullary collecting duct cells in rat.
Transcriptional profiling of native inner medullary collecting duct cells from rat kidney.
Sex, Age, Specimen part
View SamplesAPC mutant mice develop polys in the intestine, but not carcinoma. We found that additional deletion of Olfm4 gene induced carcinoma formation in the distal colon. To explore the molecular mechanism, we performed cDNA microarray to understand the gene expression files in the tumor tissues compared with WT, APC mutant and Olfm4 mutant mice.
Olfactomedin 4 deletion induces colon adenocarcinoma in Apc<sup>Min/+</sup> mice.
Sex, Age, Specimen part
View SamplesCohesin, which consists of SMC1, SMC3, Rad21 and either SA1 or SA2, topologically embraces the chromatin fibers to hold sister chromatids together and to stabilize chromatin loops. Increasing evidence indicates that these loops are the organizing principle of higher-order chromatin architecture, which in turn is critical for gene expression. To determine how cohesin contributes to the establishment of tissue-specific transcriptional programs, we compared genome-wide cohesin distribution, gene expression and chromatin architecture in cerebral cortex and pancreas from adult mice. More than one third of cohesin binding sites differ between the two tissues and these are enriched at the regulatory regions of tissue-specific genes. Cohesin colocalizes extensively with the CCCTC-binding factor (CTCF). Cohesin/CTCF sites at active enhancers and promoters contain, at least, cohesin-SA1 whereas either cohesin-SA1 or cohesin-SA2 are present at active promoters independently of CTCF. Analyses of chromatin contacts at the Protocadherin gene cluster and the Regenerating islet-derived (Reg) gene cluster, mostly expressed in brain and pancreas respectively, revealed remarkable differences in the architecture of these loci in the two tissues that correlate with the presence of cohesin. Moreover, we found decreased binding of cohesin and reduced transcription of the Reg genes in the pancreas of SA1 heterozygous mice. Given that Reg proteins are involved in the control of inflammation in pancreas, such reduction may contribute to the increased incidence of pancreatic cancer reported in these animals. Overall design: Examination of the relationship between gene expression, genome wide cohesin distribution and chromatin structure
The contribution of cohesin-SA1 to gene expression and chromatin architecture in two murine tissues.
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