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RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression [RNA-seq]

ABSTRACT: To investigate the cooperative function NCoR/HDAC3/PGC1β complex in the regulation of osteoclast differentiation, we used NCoR KO or PGC1β KO bone marrow cells and non-coding RNA Dancr/Rnu12 siRNA knockdown bone marrow cells or RAW 264.7 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE211674 | GEO | 2022/08/22

REPOSITORIES: GEO

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RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression [eCLIP-seq]

Project description:To investigate the cooperative function NCoR/HDAC3/PGC1β complex in the regulation of osteoclast differentiation, we used NCoR KO or PGC1β KO bone marrow cells and non-coding RNA Dancr/Rnu12 siRNA knockdown bone marrow cells or RAW 264.7 cells. We selected Dancr and Rnu12 as non-coding RNAs to knockdown based on results from an eCLIP essay.

2022-08-22 | GSE211675 | GEO

RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression [ChIP-seq]

Project description:To investigate the genomic localization of NCoR/HDAC3/PGC1β complex and the enhancer/promoter activity in the regulation of osteoclast differentiation, we used NCoR KO or PGC1β KO bone marrow cells, non-coding RNA Dancr/Rnu12 siRNA knockdown bone marrow cells and FLAG-tagged PGC1β RNA recognition motif deletion mutant expressed RAW 264.7 cells. We then performed chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for H3K27ac, NCoR, HDAC3, PGC1β, p65, Fosl2, PU.1 and FLAG-tag.

2022-08-22 | GSE211672 | GEO

A TLR4/Traf6-dependent signaling pathway mediates NCoR co-activator complex formation for inflammatory gene activation [ChIP-seq]

Project description:To investigate the genomic localization of NCoR/HDAC3/PGC1β complex and the enhancer/promoter activity in inflammatory genes, we used NCoR KO or PGC1β KO bone marrow-derived macrophages and Traf6 siRNA knockdown bone marrow-derived macrophages. We then performed chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for H3K27ac, NCoR, HDAC3, PGC1β, ERK1, p65, Fosl2, PU.1 and p300.

2023-12-21 | GSE247941 | GEO

A TLR4/Traf6-dependent signaling pathway mediates NCoR co-activator complex formation for inflammatory gene activation [RNA-seq]

Project description:To investigate the cooperative function NCoR/HDAC3/PGC1β complex in TLR4-regulated inflammatory genes, we used bone marrow-derived macrophages treated with or without KLA. We then performed gene expression profiling analysis using data obtained from RNA-seq.

2023-12-21 | GSE247942 | GEO

RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression [ATAC-seq]

Project description:To investigate the enhancer/promoter activity in the regulation of osteoclast differentiation, we used bone marrow cells treated with or without RANKL. We then analyzed open chromatin regions obtained from ATAC-seq data.

2022-08-22 | GSE211671 | GEO

RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression

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

2022-08-22 | GSE211676 | GEO

RANK+TLR2+ Myeloid Subpopulation Converts Autoimmune to Joint Destruction in Rheumatoid Arthritis

Project description:Joint destruction is the major clinic burden in patients with rheumatoid arthritis (RA). It is unclear, though, how this autoimmune disease progresses to the point of deterioration of the joint. Here, we report that in a mouse model of RA the upregulation of TLR2 expression and its a(2,3) sialylation in RANK+ myeloid monocytes mediate the transition from autoimmunity to osteoclast fusion and bone resorption, resulting in joint destruction. The expression of a(2,3) sialyltransferases were significantly increased in RANK+TLR2+ myeloid monocytes, and their inhibition or treatment with a TLR2 inhibitor blocked osteoclast fusion. Notably, analysis of our single-cell RNA-sequencing (scRNA-seq) libraries generated from RA mice revealed a novel RANK+TLR2- subset that negatively regulated osteoclast fusion. Importantly, the RANK+TLR2+ subset was significantly diminished with the treatments. Moreover, the RANK+TLR2- subset could differentiate into a TRAP+ osteoclast lineage, but the resulting cells did not fuse to form osteoclasts. Our scRNA-seq data showed that Maf is highly expressed in the RANK+TLR2- subset, and the a(2,3) sialyltransferase inhibitor induced Maf expression in the RANK+TLR2+ subset. The identification of a RANK+TLR2- subset provides a potential explanation for TRAP+ mononuclear cells in bone and their anabolic activity. Further, TLR2 expression and its a(2,3) sialylation in the RANK+ myeloid monocytes could be effective targets to prevent autoimmune-mediated joint destruction.

2023-05-24 | GSE221704 | GEO

lncRNAs and mRNAs expression profile in liver diseases including HCC

Project description:Sustained hepatic inflammation can contribute to cancer initiation and progression via tumor-initiating cell expansion, but underlying mechanisms remains unknown. Expression profiles of lncRNAs/mRNAs were measured in normal, chronic hepatitis, cirrhotic and cancerous livers. We found abundant disease-related lncRNAs/mRNAs deregulated across different stages of inflammation-triggered liver disease and refined a transformation gene signature to distinguish pathological liver tissues. Amongst this signature, a conserved lncRNA DANCR was silenced in normal adult liver, but overexpressed in fetal and cancerous livers. Remarkably, increased DANCR significantly correlates with poor prognosis in multiple-center cohorts and is directly induced by inflammatory pathways including NF-ÎºB and STAT3. DANCR could suppress cell differentiation and drive expansion of tumor-initiating cells, leading to chemoresistance. Moreover, in vitro and in vivo inhibition confirms the significance of DANCR as a therapeutic target when combined with other chemotherapy. We illustrate the role of DANCR relies on the regulation of CTNNB1 in a novel miRNA-blocking manner. Our studies reveal the expression of lncRNAs/mRNAs in normal and pathological livers and suggest the importance of oncofetal lncRNA DANCR in inflammation-induced malignant transformation, offering a potential prognostic marker and a therapeutic target for HCC. In the study, 10 normal livers (NL), 10 chronic inflammatory livers (IL), 10 cirrhotic livers (CL), 13 early HCC (eHCC) and 13 advanced HCC (aHCC) samples were profiled their lncRNA/mRNA expression

2014-01-22 | E-GEOD-54238 | biostudies-arrayexpress

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

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