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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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A Bcl6-Smrt/Ncor repression program controls atherosclerosis

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE27001: Inhibition of Bcl6-SMRT/NCoR interactions by an inhibitory peptide affects inflammatory pathways GSE27033: Genome-wide location analysis of SMRT and NCoR in wild-type and Bcl6 knockout macrophages Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Ruth Yu

PROVIDER: E-GEOD-27060 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The Bcl6-SMRT/NCoR cistrome represses inflammation to attenuate atherosclerosis.

Barish Grant D GD Yu Ruth T RT Karunasiri Malith S MS Becerra Diana D Kim Jason J Tseng Tiffany W TW Tai Li-Jung LJ Leblanc Matthias M Diehl Cody C Cerchietti Leandro L Miller Yury I YI Witztum Joseph L JL Melnick Ari M AM Dent Alexander L AL Tangirala Rajendra K RK Evans Ronald M RM

Cell metabolism 20120329 4

Chronic inflammation is a hallmark of atherosclerosis, but its transcriptional underpinnings are poorly understood. We show that the transcriptional repressor Bcl6 is an anti-inflammatory regulator whose loss in bone marrow of Ldlr(-/-) mice results in severe atherosclerosis and xanthomatous tendonitis, a virtually pathognomonic complication in patients with familial hypercholesterolemia. Disruption of the interaction between Bcl6 and SMRT or NCoR with a peptide inhibitor in vitro recapitulated ...[more]

PMID: 22465074

Similar Datasets

Genome-wide location analysis of SMRT and NCoR in wild-type and Bcl6 knockout macrophages

Project description:Using ChIP-seq, we reveal the SMRT and NCoR co-repressor cistromes, which each consist of over 30,000 half-shared binding sites. Moreover, we identify Bcl6-bound sub-cistromes for each co-repressor, which are strongly concentrated on NF-κB-driven inflammatory and tissue remodeling genes. These results reveal a critical role for Bcl6 and its corepressors SMRT and NCoR in the prevention of atherosclerosis and chronic inflammation. Identification of SMRT and NCoR binding sites in wild-type and Bcl6 knockout primary bone-marrow derived macrophages

2012-03-29 | E-GEOD-27033 | biostudies-arrayexpress

Inhibition of Bcl6-SMRT/NCoR interactions by an inhibitory peptide affects inflammatory pathways

Project description:Using microarrays, we compared the changes in levels of gene expression between wild type mouse bone marrow derived macrophages upon treatment with the Bcl6 peptide inhibitor, RI-BPI, that specifically blocks interaction between BCL6 and the co-repressors NCoR or SMRT. Total RNA was obtained from cultered wild type primary bone marrow-derived macrophages that were treated with either 5 μM control or RI-BPI peptide in MSF media for 12 hours.

2012-03-29 | E-GEOD-27001 | biostudies-arrayexpress

Genome-wide location analysis of SMRT and NCoR in wild-type and Bcl6 knockout macrophages

2012-03-30 | GSE27033 | GEO

Inhibition of Bcl6-SMRT/NCoR interactions by an inhibitory peptide affects inflammatory pathways

2012-03-30 | GSE27001 | GEO

CDDP treatment of U2OS cells with NCOR and SMRT knock-down

Project description:We detected an interaction between checkpoint kinase Chk2 and some members of the NCOR/SMRT co-repressor complex. In order to study the role of gene repression in the checkpoint response to DNA damage, we performed RNA profiling in NCOR or SMRT knockdown cells after treztment with cisplatin. U2OS cells were transfected with siRNAs for NCOR or SMRT, grown for 2 days in complete medium, and then treated with 100 microM cisplatin (CDDP) for 6h. Biological duplicates were used for RNa profiling

2012-02-06 | E-GEOD-34226 | biostudies-arrayexpress

CDDP treatment of U2OS cells with NCOR and SMRT knock-down

2012-02-06 | GSE34226 | GEO

NCoR/SMRT co-repressors cooperate with c-MYC to create an epigenetic barrier to somatic cell reprogramming [RNA-seq]

Project description:Changing the somatic cell transcriptome to a pluripotent state using exogenous reprogramming factors needs transcriptional co-regulators that help activate or suppress gene expression and rewrite the epigenome. Here, we show that reprogramming-specific engagement of the NCoR/SMRT co-repressor complex at key pluripotency loci creates an epigenetic block to reprogramming. HDAC3 executes the repressive function of NCoR/SMRT in reprogramming by inducing histone deacetylation at these loci. Recruitment of NCoR/SMRT-HDAC3 to pluripotency genes is facilitated by all 4 Yamanaka factors (OCT4, SOX2, KLF4 and c-MYC) but mostly by c-MYC. Class IIa HDACs further potentiate this recruitment by interacting with both the reprogramming factors and NCoR/SMRT. Consequently, depleting NCoR/SMRT-HDAC3 function enables high efficiency of reprogramming, while elevating NCoR/SMRT-HDAC3 recruitment at pluripotency loci by over-expressing constitutively active class IIa HDACs derails it. Our findings thus uncover an unexpected epigenetic mechanism involving c-MYC, whose manipulation greatly enhances reprogramming efficiency.

2018-03-07 | GSE70738 | GEO

NCoR/SMRT co-repressors cooperate with c-MYC to create an epigenetic barrier to somatic cell reprogramming [ChIP-Seq]

2018-03-07 | GSE70736 | GEO

GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.

Project description:NCoR and SMRT are two paralogous vertebrate proteins that function as corepressors with unliganded nuclear receptors. Although C. elegans has a large number of nuclear receptors, orthologues of the corepressors NCoR and SMRT have not unambiguously been identified in Drosophila or C. elegans. Here, we identify GEI-8 as the closest homologue of NCoR and SMRT in C. elegans and demonstrate that GEI-8 is expressed as at least two isoforms throughout development in multiple tissues, including neurons, muscle and intestinal cells. We demonstrate that a homozygous deletion within the gei-8 coding region, which is predicted to encode a truncated protein lacking the predicted NR domain, results in severe mutant phenotypes with developmental defects, slow movement and growth, arrested gonadogenesis and defects in cholinergic neurotransmission. Whole genome expression analysis by microarrays identified sets of de-regulated genes consistent with both the observed mutant phenotypes and a role of GEI-8 in regulating transcription. Interestingly, the upregulated transcripts included a predicted mitochondrial sulfide:quinine reductase encoded by Y9C9A.16. This locus also contains non-coding, 21-U RNAs of the piRNA. Inhibition of the expression of the region coding for 21-U RNAs leads to irregular gonadogenesis in the homozygous gei-8 mutants, but not in an otherwise wild-type background, suggesting that GEI-8 may function in concert with the 21-U RNAs to regulate gonadogenesis. Our results confirm that GEI-8 is the orthologue of the vertebrate NCoR/SMRT corepressors and demonstrate important roles for this putative transcriptional corepressor in development and neuronal function. Comparison of Mutant vs. WT control with three replications per treatment group

2013-08-11 | E-GEOD-40127 | biostudies-arrayexpress

GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.

2013-08-11 | GSE40127 | GEO

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