Project description:This SuperSeries is composed of the following subset Series: GSE29606: Gene expression profiles of effector T cells induced by mTOR inhibition GSE29607: Comparison of gene expression profiles of effector T cells from leptin-receptor-deficient mice and wild type mice Refer to individual Series
Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed during leptin receptor deficiency, which is partly responsible for the inhibition of T cell effector functions. Mouse CD4+CD25- T cells were purified from leptin-receptor-deficient mice and wild type mice, and stimulated with anti-CD3 and anti-CD28 for 12h. Six mice of each genotype were used. Leptin receptor deficiency-induced gene expression profiles were evaluated in mouse effector T cells from db/db mice and compared to the ones observed in their WT counterpart (db/+ mice). Two independent experiments were performed, and in each of them, 3 mice/group were pooled.
Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed during leptin receptor deficiency, which is partly responsible for the inhibition of T cell effector functions. Mouse CD4+CD25- T cells were purified from leptin-receptor-deficient mice and wild type mice, and stimulated with anti-CD3 and anti-CD28 for 12h. Six mice of each genotype were used.
Project description:Leptin deficient mice is an appealing model for studying of metabolic syndromes. In this data, we provide 7 different tissues’ RNA-seq reads for each leptin-deficient mice (ob/ob) and wild type mice.
Project description:Leptin-responsive genes in the pathway of a leptin signal from the hypothalamus to the liver has not been detected. We used microarray to detailed the expression of gene in liver in the status of leptin deficiency, and leptin administration. As leptin deficient status, we use Lepmkyo/Lepmkyo rats or Lepob/Lepob mice and their wild type littermates.
Project description:We employed translating ribosome affinity purification followed by RNA sequencing to isolate and analyze mRNA from the hypothalamic LepRb neurons of wild-type or leptin-deficient (Lepob/ob) mice treated with vehicle or exogenous leptin. Although the expression of most of the genes encoding the neuropeptides commonly considered to represent the main targets of leptin action were altered only following chronic leptin deprivation, our analysis revealed other transcripts that were coordinately regulated by leptin under multiple treatment conditions. Among these, acute leptin treatment increased expression of the transcription factor Atf3 in LepRb neurons.
Project description:TAZ-deficient mice have the abnormalities in the lung development. We expect the comparison of the gene expression profiles of TAZ-deficient and wild-type lungs would reveal the underlying mechanisms. Keywords: genetic modification
Project description:In several models of obesity-induced diabetes, increased lipid accumulation in the liver has been associated with decreased diabetes susceptibility. For instance, deficiency in leptin receptor (db/db) leads to hyperphagia and obesity in both C57BL/6 and C57BLKS mice but, only on the C57BLKS background do the mice develop beta-cell loss leading to severe diabetes while C57BL/6 mice are relatively resistant. Liver triglyceride levels in the resistant C57BL/6 mice are 3 to 4 fold higher than in C57BLKS. To better understand the mechanisms contributing to metabolic dysfunction in obesity-induced diabetes, we used microarrays to comprehensively profile gene expression livers of F2 mice (B57BL/6 X DBA/2) deficient in leptin receptor (db/db) DBA/2J females were mated to C57BL/6 males carrying leptin receptor deficiency (db/+) and, F1 (db/+) offspring were interbred to produce F2 mice. Offspring deficient in leptin receptor (db/db) were fed on a chow diet until 5 weeks or 12 weeks of age and then euthanized for collection of liver tissue for RNA profiling along with other diabetes-related phenotypes.
