Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA357600 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5114004.fastq.gz | Fastqsanger.gz | |||
| SRR5114005.fastq.gz | Fastqsanger.gz | |||
| SRR5114006.fastq.gz | Fastqsanger.gz | |||
| SRR5114007.fastq.gz | Fastqsanger.gz | |||
| SRR5114008.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Nuclear receptor corepressor (NCOR) and HDAC3 in hypothalamus [ChIP-Seq]
| PRJNA357599 | ENA
Project description:Nuclear receptor corepressor (NCOR) and HDAC3 in hypothalamus
| PRJNA357597 | ENA
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.
2018-10-29 | GSE92451 | GEO
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.
2018-10-29 | GSE92450 | GEO
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
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 | GSE250040 | GEO
Project description:We profiled gene expression in livers depleted of NCOR (nuclear receptor corepressor) along with wild-type livers as control. NCOR floxed mice were intravenously injected with adeno-associated virus (AAV) expressing Cre or GFP. Livers were harvested at 2-weeks post-injection at 5pm (ZT10). Total RNA was extracted and hybridized to Affymetrx Mouse Gene 2.0 array.
2013-11-25 | E-GEOD-49387 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) is a key thermogenic organ, whose expression of Uncoupling Protein 1 (UCP1) and ability to maintain body temperature in response to acute cold exposure requires histone deacetylase 3 (HDAC3). HDAC3 exists in tight association with nuclear receptor corepressors NCoR1 and NCoR2(also known as Silencing Mediator of Retinoid and Thyroid Receptors, or SMRT), butthe functions of NCoR1/2 in BAT have not been established.Here we report that, as expected, genetic loss of NCoR1/2 in BAT (NCoR1/2 BAT-dKO) leads to loss of HDAC3 activity. In addition, HDAC3 is no longer bound at its physiological genomic sites in the absence of NCoR1/2, leading to a shared deregulation of BAT lipid metabolism between the NCoR1/2 BAT-dKO and HDAC3 BAT KO mice. Despite these commonalities, however, loss of NCoR1/2 in BAT does not phenocopy the cold sensitivity observed in the HDAC3 BAT-KO, nor does loss of either corepressor alone. Instead, BAT lacking NCoR1/2 is inflamed, particularly with respect to the IL-17 axis that increases thermogenic capacity by enhancing innervation. Integration of BAT RNA-seq and ChIP-seq data revealed that NCoR1/2 directly regulate Mmp9, which integrates extracellular matrix remodeling and inflammation. These findings reveal pleiotropic functions of the NCoR/HDAC3 corepressor complex in BAT, such that HDAC3-independent suppression of BAT inflammation counterbalances their stimulation of HDAC3 activity in the control of thermogenesis.
2022-07-27 | GSE199808 | GEO
Project description:We profiled gene expression in livers depleted of NCOR (nuclear receptor corepressor) along with wild-type livers as control.
2013-11-25 | GSE49387 | GEO
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