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The global IL-1α gene expression response in p65 enhancer mutant HeLa cells.

ABSTRACT: The global IL-1α gene expression response in p65 enhancer mutant HeLa cells.

PROVIDER: PRJNA565974 | ENA |

REPOSITORIES: ENA

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The global IL-1α gene expression response in p65 enhancer mutant HeLa cells.

Project description:Conversion of cytokine-driven changes in chromatin topology into gene regulatory circuits during inflammation still remains unclear. Here, we analyzed the expression profiles of HeLa cells carrying microdeletions of p65-binding sites in two enhancers regulating the IL-1α-inducible IL8 and CXCL1-3 genes within the extended chemokine locus on human chromosome 4.

2019-09-18 | GSE137589 | GEO

Genome-wide TNFM-NM-1-induced p65 binding before and after telomerase inhibition in HeLa cells

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) was performed to analyze the effect of telomerase inhibition on TNFM-NM-1-induced genome-wide p65 binding in HeLa cells. By obtaining over 40 million uniquely mappable reads per sample from ChIP-seq, maps for TNFM-NM-1-induced p65 binding in absence and presence of an hTERT inhibitor, MST-312, were generated. As expected, TNFM-NM-1 treatment significantly increased genome-wide p65 occupancy. Interestingly, when cells were treated with MST-312 prior to TNFM-NM-1 stimulation, the number of p65 binding sites was reduced. In addition, some binding sites, including important p65 targets like IL6 and TNF, showed a reduced p65 occupancy with a minimum fold change of 1.5, after MST-312 exposure. Taken together, our ChIP-seq data indicate that telomerase is required for optimal p65 binding at a small proportion of p65 target sites upon inflammatory stimuli. Examination of p65 binding in HeLa cells in absence and presence of TNFM-NM-1 and MST-312.

2012-11-26 | E-GEOD-41100 | biostudies-arrayexpress

Timecourse of gene expression in HeLa cells (parental cells and clonal knockouts of MED12 and MED24) following induction by TNFa or IL-1b

Project description:Activation of nuclear factor kappa B (NF-kB) by inflammatory signals results in nuclear translocation of the transcription factor p65 and induction of gene expression. We identified MED12 and MED24 in an optical pooled CRISPR knockout screen in HeLa-Cas9 cells for genes affecting the activation and/or relaxation of p65 to the cytoplasm following induction by either TNFa or IL-1b. We generated isogenic clonal knockout HeLa-Cas9 lines using crRNA transfection and confirmed that loss of MED12 or MED24 results in delayed relaxation of p65, assayed by live-cell imaging of a p65-mNeonGreen fluorescent fusion.

2019-10-01 | GSE132704 | GEO

IL-1 versus p65 overexpression [human, rat]

Project description:IL-1 versus p65 overexpression [human, rat]

| PRJNA510929 | ENA

Characterization of IL-1α–responsive enhancers and of IL-1α -mediated changes in chromatin topology.

Project description:Characterization of IL-1α–responsive enhancers and of IL-1α -mediated changes in chromatin topology.

| PRJNA555101 | ENA

Genome-wide TNFα-induced p65 binding before and after telomerase inhibition in HeLa cells

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) was performed to analyze the effect of telomerase inhibition on TNFα-induced genome-wide p65 binding in HeLa cells. By obtaining over 40 million uniquely mappable reads per sample from ChIP-seq, maps for TNFα-induced p65 binding in absence and presence of an hTERT inhibitor, MST-312, were generated. As expected, TNFα treatment significantly increased genome-wide p65 occupancy. Interestingly, when cells were treated with MST-312 prior to TNFα stimulation, the number of p65 binding sites was reduced. In addition, some binding sites, including important p65 targets like IL6 and TNF, showed a reduced p65 occupancy with a minimum fold change of 1.5, after MST-312 exposure. Taken together, our ChIP-seq data indicate that telomerase is required for optimal p65 binding at a small proportion of p65 target sites upon inflammatory stimuli.

2012-11-26 | GSE41100 | GEO

Analysis of p65 genomic location changes with IL-17 blockade

Project description:We characterize the effect that IL-17 blockade has on p65 genomic location in epidermal aged cells

2023-03-24 | GSE213732 | GEO

CD44 plays a key role in aggravating tubular cell apoptosis in renal ischemia-reperfusion injury through p65/ PGC-1α pathway

Project description:Acute kidney injury (AKI) is rapidly increasing and becomes a major of public health problem nowadays. However, its underlying mechanism has not been elucidated. Studies have shown that cluster of differentiation-44 (CD44) play a role in the pathological process of AKI. Nevertheless, the molecule mechanism has not been totally clarified. Herein, we found that CD44 is increased in renal tubules in ischemia-reperfusion injury (IRI)-induced AKI mice. Knockout of CD44 improved mitochondrial biogenesis and mitochondrial fatty acid oxidation (FAO), further protecting against renal tubular cell apoptosis and kidney injury. Conversely, ectopic expression of CD44 impaired mitochondrial function and FAO, which exacerbated the pathological process of AKI. Transcriptome sequencing revealed NF-κB p65 is highly responsible for this process. In vitro, we found that CD44 induced activation of NF-κB p65 via mitogen-activated protein kinase (MAPK) ERK1/2 and MAPK p38, further transcriptionally silencing peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) promoters. As a result, downregulation of PGC-1α contributed to impairment of mitochondrial dysfunction and FAO, resulting in the deterioration of AKI. Our study found that inhibiting CD44 is a new potential therapeutic strategy for AKI through promoting mitochondrial biogenesis and FAO. The underlying mechanism is associated with MAPK/p65/ PGC-1α pathway.

2025-02-26 | GSE252060 | GEO

The activation of IL-1 induced enhancers depends on TAK1 kinase activity and NF-KB p65 [RNA-Seq]

Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-?B subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-?B p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-?B-dependent enhancers in epithelial cells. RNA-seq of KB cells either untreated or treated with IL-1 alpha

2014-12-16 | E-GEOD-64185 | biostudies-arrayexpress

p65

Project description:p65

| PRJNA811604 | ENA