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Unknown,Transcriptomics,Genomics,Proteomics

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HNF6 and Rev-erba Integrate Hepatic Lipid Metabolism By Overlapping and Distinct Transcriptional Mechanisms

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Bin Fang

PROVIDER: E-GEOD-83791 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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HNF6 and Rev-erba Integrate Hepatic Lipid Metabolism By Overlapping and Distinct Transcriptional Mechanisms [Affymetrix]

Project description:We address the function of HNF6 in the mouse liver metabolism and Rev-erba cistrome We performed microarray in mouse livers at 5pm of the day and compared between WT and HNF6-depleted livers.

2016-06-29 | E-GEOD-83789 | biostudies-arrayexpress

HNF6 and Rev-erba Integrate Hepatic Lipid Metabolism By Overlapping and Distinct Transcriptional Mechanisms [ChIP-Seq]

Project description:We address the function of HNF6 in the mouse liver metabolism and Rev-erba cistrome We performed Rev-erba ChIP-seq in mouse livers at 5pm of the day and compared between WT and HNF6-depleted livers.

2016-06-29 | E-GEOD-83790 | biostudies-arrayexpress

HNF6 and Rev-erba Integrate Hepatic Lipid Metabolism By Overlapping and Distinct Transcriptional Mechanisms

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-06-29 | GSE83791 | GEO

HNF6 and Rev-erba Integrate Hepatic Lipid Metabolism By Overlapping and Distinct Transcriptional Mechanisms [Affymetrix]

Project description:We address the function of HNF6 in the mouse liver metabolism and Rev-erba cistrome

2016-06-29 | GSE83789 | GEO

HNF6 and Rev-erba Integrate Hepatic Lipid Metabolism By Overlapping and Distinct Transcriptional Mechanisms [ChIP-Seq]

Project description:We address the function of HNF6 in the mouse liver metabolism and Rev-erba cistrome

2016-06-29 | GSE83790 | GEO

HNF6 and Rev-erbα integrate hepatic lipid metabolism by overlapping and distinct transcriptional mechanisms.

Project description:Hepatocyte nuclear factor 6 (HNF6) is required for liver development, but its role in adult liver metabolism is not known. Here we show that deletion of HNF6 in livers of adult C57Bl/6 mice leads to hepatic steatosis in mice fed normal laboratory chow. Although HNF6 is known mainly as a transcriptional activator, hepatic loss of HNF6 up-regulated many lipogenic genes bound directly by HNF6. Many of these genes are targets of the circadian nuclear receptor Rev-erbα, and binding of Rev-erbα at these sites was lost when HNF6 was ablated in the liver. While HNF6 and Rev-erbα coordinately regulate hepatic lipid metabolism, each factor also affects additional gene sets independently. These findings highlight a novel mechanism of transcriptional repression by HNF6 and demonstrate how overlapping and distinct mechanisms of transcription factor function contribute to the integrated physiology of the liver.

| S-EPMC4973293 | biostudies-literature

HNF6 and Rev-erba Integrate Hepatic Lipid Metabolism By Overlapping and Distinct Transcriptional Mechanisms

Project description:HNF6 and Rev-erba Integrate Hepatic Lipid Metabolism By Overlapping and Distinct Transcriptional Mechanisms

| PRJNA327023 | ENA

Circadian Epigenomic Control of Skeletal Muscle Fuel Metabolism by HDAC3

Project description:We address the function of HDAC3 in skeletal muscle metabolism We performed HDAC3 ChIP-seq, RNA-seq, and GRO-seq in mouse muscles at different times of the day and compared between WT and HDAC3-depleted muscles.

2016-09-06 | E-GEOD-79696 | biostudies-arrayexpress

REV-ERBa regulates TH17 cell development and autoimmunity

Project description:RORγt is well recognized as the lineage defining transcription factor for TH17 cell development. However, the cell-intrinsic mechanisms that negatively regulate TH17 cell development and autoimmunity remain poorly understood. Here we demonstrate that the transcriptional repressor REV-ERBa is exclusively expressed in TH17 cells, competes with RORγt for their shared DNA consensus sequence, and negatively regulates TH17 cell development via repression of genes traditionally characterized as RORγt-dependent, including Il17a. Deletion of REV-ERBa enhanced TH17-mediated pro-inflammatory cytokine expression, exacerbating experimental autoimmune encephalomyelitis (EAE) and colitis. Treatment with REV-ERB-specific synthetic ligands, which have similar phenotypic properties as RORγ modulators, suppressed TH17 cell development, was effective in colitis intervention studies, and significantly decreased the onset, severity, and relapse rate in several models of EAE without affecting thymic cellularity. Our results establish that REV-ERBa negatively regulates pro-inflammatory TH17 responses in vivo and identifies the REV-ERBs as potential targets for the treatment of TH17-mediated autoimmune diseases.

2018-12-19 | GSE122726 | GEO

KLF15 dependent REV-ERBa binding in the heart

Project description:By comparing the ChIPseq signal of REV_ERBa in control (Flox) and cardiomyocytic KLF15 knockout (cKO), we identified the KLF15 dependent REV-ERBa binding and repression in the heart. We further compared the differential binding sites to KLF15 binding site, using a FLAG tagged cardiomyocytic transgenic (cTG1) mice.

2015-12-30 | GSE73741 | GEO

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