Bcl3 target genes in mESCs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE70246 | GEO | 2015/06/25
SECONDARY ACCESSION(S): PRJNA288030
REPOSITORIES: GEO
Similar Datasets
Project description:Bcl3 is expressed in mESCs. ChIP-seq was used to identify its binding pattern and target genes. ChIP of Bcl3 in mESCs under conventional culture condition
2015-06-25 | E-GEOD-70246 | biostudies-arrayexpress
Project description:B-cell lymphoma 3-encoded protein (Bcl3) is an intimate and context-specific regulator of the NF-kB family of transcription factors, a ubiquitous master regulator involved in many homeostatic and inflammatory processes. NF‑kB signalling determines the fates of bone-forming osteoblasts and bone-resorbing osteoclasts. Herein we show that Bcl3 is a negative regulator of NF‑kB via control of osteoblast and osteoclast function. Mice lacking Bcl3 (Bcl3−/−) have congenitally increased bone density, long bone dwarfism, increased biomechanical strength and altered bone turnover. Bcl3−/− osteoblasts and osteoclasts have accelerated differentiation and increased activity; whereas, rescue overexpression with a Bcl3 mimetic peptide inhibits differentiation. Early-differentiating Bcl3−/− osteoblasts have altered gene transcription favouring bone formation, including perturbation of the RANKL-OPG axis. In a model of osteoarthritic aberrant mineralisation Bcl3−/− mice exhibit decreased pathological osteophyte formation. Cumulatively, these findings identify Bcl3 as a viable target for controlling NF‑kB signalling in the treatment of skeletal pathologies.
2019-01-17 | GSE125153 | GEO
Project description:By binding to specific DNA elements, known collectively as “κB sites”, contained within the promoters/enhancers of target genes, NF-κB regulates gene expression. We found that the identity of the central base pair (bp) of κB sites profoundly impacts the transcriptional activity of NF-κB dimers. RelA dimers prefer an A/T bp at this position for optimum transcriptional activation (A/T-centric) and discriminate against G/C-centric κB sites. The p52 homodimer, in contrast, activates transcription from G/C-centric κB sites in complex with Bcl3 but represses transcription from the A/T-centric sites. The p52:Bcl3 complex binds to these two classes of κB sites in distinct modes permitting recruitment of coactivator, corepressor, or both coactivator and corepressor complexes in promoters containing G/C, A/T or both G/C and A/T-centric sites. Therefore, through sensing of bp differences within κB sites, NF-κB dimers modulate biological programs by activating, repressing and altering expression of effector genes. Total RNA extracted from bone marrow derived macrophages (BMDMs) with Bcl3 siRNA knockdown or mouse scramble siRNA knockdown were subjected to LPS stimulation.
2012-08-06 | E-GEOD-39922 | biostudies-arrayexpress
Project description:Peripherally induced regulatory T cells (pTregs) expressing the retinoic acid receptor-related orphan-receptor gamma t (RORγt) are indispensable for intestinal immune homeostasis. Previous studies have determined the role of the atypical NFκB inhibitor Bcl3 in the development of colitis. In this study we analyzed the influence of Bcl3 on pTreg development and functionality in healthy mice and under colitogenic conditions. Our findings reveal that expression of Bcl3, in health, limits not just the development of pTregs in a T cell intrinsic manner but also the formation of a RORγt+Helios+ double positive subset (DPTreg) expressing an activated transcriptional profile. Consequently, loss of Bcl3 in Tregs does not impede their suppressive capacity in a model of T cell transfer colitis but moreover leads to increased production of anti-inflammatory cytokines IL-10 and TGFβ. We further demonstrate that lack of Bcl3 in Tregs results in trans-differentiation towards Th17-like cells. Finally, we provide a Bcl3 dependent gene signature in pTregs including altered signaling of the cytokines IL-2, IL-6 and TNFα. We therefore conclude that expression of Bcl3 regulates the sensitivity of Tregs towards homeostatic cytokines and consequently limits the formation of an unphysiological number of RORγt+ Tregs.
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Project description:We identify the atypical inhibitor-κB protein, Bcl3, as a novel biomarker in gliomas whose expression level predicts response to therapy. Bcl3 is found at 19q13 and its expression level in glioma is regulated by copy number alteration. Mechanistically, Bcl3 mediates mesenchymal differentiation and its presence promotes resistance to cytotoxic DNA damage.
2018-07-21 | GSE80729 | GEO
Project description:In this assay, we aimed to investigate whether ZFP661 co-binds target regions with CTCF. To achieve this, we performed ChIP-reChIP-seq in ZFP661-3HA overexpressing (OE) mESCs, where the 1st ChIP utilized anti-HA antibody, and the 2nd ChIP involved the use of anti-IgG and anti-CTCF antibodies, respectively. Our results demonstrate that ZFP661 co-binds target regions with CTCF.
2023-05-09 | GSE231865 | GEO
Project description:Genome-wide occupancy of biotinylated Jmjd2b, Jmjd2c from mESCs, as well as occupancy of selected factors and histone marks from wild-type mESCs, Anti-GFP KD, Jmj2b KD and Jmjd2c KD mESCs genome To identify genome-wide binding target sites of Jmjd2b and Jmjd2c in the mESCs genome, and genome-wide binding sites for selected factors and histone marks from Anti-GFP KD, Jmjd2b KD and Jmjd2c KD mESCs
2013-12-01 | E-GEOD-43229 | biostudies-arrayexpress
Project description:By binding to specific DNA elements, known collectively as “κB sites”, contained within the promoters/enhancers of target genes, NF-κB regulates gene expression. We found that the identity of the central base pair (bp) of κB sites profoundly impacts the transcriptional activity of NF-κB dimers. RelA dimers prefer an A/T bp at this position for optimum transcriptional activation (A/T-centric) and discriminate against G/C-centric κB sites. The p52 homodimer, in contrast, activates transcription from G/C-centric κB sites in complex with Bcl3 but represses transcription from the A/T-centric sites. The p52:Bcl3 complex binds to these two classes of κB sites in distinct modes permitting recruitment of coactivator, corepressor, or both coactivator and corepressor complexes in promoters containing G/C, A/T or both G/C and A/T-centric sites. Therefore, through sensing of bp differences within κB sites, NF-κB dimers modulate biological programs by activating, repressing and altering expression of effector genes.
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