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GPS2 and HDAC3 RNA-Seq in GPS2-KO MCF-7 [RNA-Seq]

ABSTRACT: GPS2 and HDAC3 RNA-Seq in GPS2-KO MCF-7 [RNA-Seq]

PROVIDER: PRJNA1051984 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27198027_1.fastq.gz	Fastqsanger.gz
	SRR27198027_2.fastq.gz	Fastqsanger.gz
	SRR27198028_1.fastq.gz	Fastqsanger.gz
	SRR27198028_2.fastq.gz	Fastqsanger.gz
	SRR27198029_1.fastq.gz	Fastqsanger.gz

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GPS2 and HDAC3 ChIP-Seq and RNA-Seq in GPS2-KO MCF-7

Project description:GPS2 and HDAC3 ChIP-Seq and RNA-Seq in GPS2-KO MCF-7

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GPS2 and HDAC3 ChIP-Seq in GPS2-KO MCF-7 [ChIP-Seq]

Project description:GPS2 and HDAC3 ChIP-Seq in GPS2-KO MCF-7 [ChIP-Seq]

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GPS2 and HDAC3 RNA-Seq in GPS2-KO MCF-7 [RNA-Seq]

Project description:Within the nucleus, G-Protein Pathway Suppressor 2 (GPS2) was first recognized as a component of the core NCoR/SMRT corepressor complex. This is a multi-protein complex that functions as a corepressor for a variety of transcription factors, including nuclear receptors, and promotes the deacetylation of histones on target regulatory regions via its main catalytic unit, the histone deacetylase HDAC3. Based on this association, GPS2 was initially characterized as a transcriptional corepressor, with transcriptomic analysis of various KO/KD models confirming its role in contributing to the repression of inflammatory genes targeted by the NCoR/SMRT complex. To address this knowledge gap, we asked whether GPS2's dual role in transcription could be attributed to the stabilization of distinct chromatin remodeling factors, with the hypothesis that stabilization of other enzymes may, in turn, affect post-transcriptional modification of histone marks in different directions. In particular, we investigated whether GPS2 presence in the NCoR/SMRT complex may prevent HDAC3 ubiquitination. Our results confirmed that lack of GPS2 leads to aberrant HDAC3 ubiquitination and its dismissal for its target genes.

2025-05-05 | GSE250075 | GEO

GPS2 and HDAC3 ChIP-Seq in GPS2-KO MCF-7 [ChIP-Seq]

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Transcriptome comparison between WT and GPS2 liver knockout (LKO) livers and GPS2 NCOR PPARa cistrome and epigenome analysis in livers.

Project description:Obesity-associated lipid overload triggers non-alcoholic fatty liver diseases (NAFLD), which in part may be driven by alterations of regulatory transcription networks and hepatocyte-selective epigenomes. Here we demonstrate that G protein pathway suppressor 2 (GPS2), a subunit of the nuclear receptor corepressor (NCOR)/ histone deacetylase 3 (HDAC3) complex, is a central component of such networks and accelerates the progression of non-alcoholic steatohepatitis (NASH). In hepatocyte-specific Gps2 knockout mice, loss of GPS2 alleviated the development of diet-induced steatosis and fibrosis and caused activation of lipid catabolic genes. By determining differential cistromes, epigenomes and transcriptomes in wild-type, single and double knockout mice, we identified the lipid-sensing nuclear receptor PPARa as a direct target of GPS2. We also provide evidence that in hepatocytes, unlike in macrophages, GPS2 acts in concert with the NCOR subunit of the corepressor complex. By analyzing the liver transcriptomes of human patients, we found that GPS2 expression positively correlated with the expression of NASH/fibrosis signature genes. Collectively, our data suggest that the GPS2-PPARa partnership in hepatocytes may influence the development of NASH/fibrosis in mice and in humans.

2019-03-12 | GSE113157 | GEO

A protective strategy against hyperinflammatory responses requiring the non-transcriptional actions of GPS2

Project description:The association between hyper-inflammatory states and numerous diseases is widely recognized, but our understanding of the molecular strategies that have evolved to prevent uncontrolled activation of inflammatory responses remains incomplete. Here, we report a critical, non-transcriptional role of GPS2 as a guardian against hyperstimulation of TNFA-induced gene program. GPS2 cytoplasmic actions are required to specifically modulate RIP1 ubiquitylation and JNK activation by inhibiting TRAF2/Ubc13 enzymatic activity. In vivo relevance of GPS2 anti-inflammatory role is confirmed by inhibition of TNFA target genes in macrophages and by improved insulin signaling in the adipose tissue of aP2-GPS2 transgenic mice. As the non-transcriptional role is complemented by GPS2 functioning as positive and negative cofactor for nuclear receptors, in vivo overexpression also results in elevated circulating level of resistin and development of hepatic steatosis. Together, these studies define GPS2 as a molecular guardian required for precise control of inflammatory responses involved in immunity and homeostasis. RNA-sequencing of polyA selected RNA molecules in 293T cells and ChIP-seq of GPS2, TBL1, and NCOR.

2012-03-23 | E-GEOD-35197 | biostudies-arrayexpress

GPS2 and HDAC3 ChIP-Seq and RNA-Seq in GPS2-KO MCF-7

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

2025-05-05 | GSE250076 | GEO

Nuclear receptor corepressor (NCOR) and HDAC3 in hypothalamus [RNA-Seq]

Project description:We determined genomic binding of HDAC3 in mouse hypothalamus by ChIP-seq, and identified target genes of the NCOR/HDAC3 complex in hypothalamus of NS-DADm (mutated deacetylase activation domain in NCORs) mice by RNA-seq.

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Total nucleoplasmic RNA-seq in MCF-7

Project description:Total nucleoplasmic RNA-seq in MCF-7

| PRJNA432953 | ENA

GPS2 cistrome analysis in BMDMs and RAW264.7 cells and epigenome comparison between WT and GPS2-knockout BMDMs.

Project description:GPS2 binding sites in BMDMs can be localized specially in enhancers (H3K27ac) and promoters (H3K27ac, H3K4me3). Upon GPS2 knock-out in BMDMs, de-repression of certain inflammatory genes occur, as accompanied by increased recruitment of H3K27ac and H3K4me3 marks.

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