Project description:Fenofibrate is a specific agonist of the nuclear receptor PPARa. To identify the gene expression under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice. We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice. There are 36 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 14 week-old from the same genetic background (C57Bl/6J) treated with Fenofibrate (100 mg/kg/day) or vehicle (aqueous solution of gum Arabic 3%) by daily gavage for 10 days. n= 4 mice for LKO, LWT and WT genotypes treated with vehicle; n=3 for KO mice treated with vehicle; n=5 mice for LWT, LKO and KO genotypes treated with fenofibrate; n=4 WT mice treated with fenofibrate. All mice were sacrified at ZT14.
Project description:Co-chaperone protein CAR Cytoplasmic Retention Protein (CCRP) interacts with various nuclear receptors and determines their localization. However, there is limited information about in vivo role of CCRP especially in nuclear receptor-mediated gene regulation. We have generated CCRP global knockout (KO) mouse and have employed whole genome microarray analysis to reveal the role of CCRP in gene regulation in the mouse liver treated with phenobarbital (CAR activator) or non-treated. Male WT and KO mice were fasted for 24 h followed by the treatment with phenobarbital or vehicle PBS for 6h. Phenobarbital significantly induced or repressed 1302 and 2744 genes in WT and KO, respectively. Interestingly, cholesterol synthesizing genes were significantly up-regulated in KO even without treatment.
Project description:NF-E2-related factor 2 (Nrf2), a transcription factor activated by oxidative stress, induces phase II conjugating or antioxidant enzymes. In the present study, we examined the effect of Nrf2 knockout (Nrf2 KO) on the kidney injury induced by cisplatin using cDNA microarray analyses. A transcriptomic approach enabled us to extract gene clusters which show significantly different mRNA expression patterns between wild type (WT) and Nrf2 KO mice. In the experimental set, WT vehicle (WT-Veh) and WT cisplatin (WT-Cis) groups were included in our previous GEO database (GSE35257) because the two groups were simultaneously shared with Nrf2 KO vehicle (Nrf2 KO-Veh) and Nrf2 KO cisplatin (Nrf2 KO-Cis) groups in the current report. Copyright (c) 2012 by Korea Food & Drug Administration.
Project description:This experiment consists of RNAseq of liver harvested from CDAHFD mice treated for 8 weeks with either the MGAT2 inhibitor compound BMS-963272 (N = 10) or with vehicle (N = 10).
Project description:This experiment consists of RNAseq of liver harvested from CDAHFD mice treated for 8 weeks with either the MGAT2 inhibitor compound BMS-963272 (N = 10) or with vehicle (N = 10).
Project description:Global gene expression profiles in brains of WT mice treated with vehicle, CGG KI mice treated with vehicle, and CGG KI mice treated with 5-ALA