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H3K27ac and p300 cut&run experiment in G549 (Injury-response/Mesenchymal GSC) cell line

ABSTRACT: EP300 was identified as potential regulator of Injury-response/Mesenchymal state in Glioblastoma stem cells. Our objective was to evaluate the effect of EP300_KO on H3K27Ac within the genome in Injury-response GSC. Moreover, we aimed to identify the p300 binding sites in Injury-response GSC to further assess how it regulates the Injury-response state.

ORGANISM(S): Homo sapiens

PROVIDER: GSE290646 | GEO | 2026/01/23

REPOSITORIES: GEO

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H3K27ac and p300 cut&run experiment in G549 (Injury-response/Mesenchymal GSC) cell line

Project description:H3K27ac and p300 cut&run experiment in G549 (Injury-response/Mesenchymal GSC) cell line

| PRJNA1229476 | ENA

G549 EP300_KO RNA-seq

Project description:EP300 was identified as potential regulator of Injury-response/Mesenchymal state in Glioblastoma stem cells. Our objective was to identify the effect of EP300 KO on transcriptomic signature of Injury-response/Mesenchymal GSC.

2026-01-23 | GSE290575 | GEO

Genome-wide assessment of differential roles for p300 and CBP in transcription regulation

Project description:Through ChIP-Seq analysis with the Illumina Whole Genome Analyzer, we identify binding sites for P300 (EP300) and CBP (CREBBP) in Human glioblastoma T98G cells that were cell cycle synchronized before and after stimulation. In our analysis, we focused on the identification of genes differentially bound by P300 and CBP. ChIP-seq with P300 and CBP antibodies over 2 timepoints

2010-03-30 | E-GEOD-21026 | biostudies-arrayexpress

Acetytransferase P300 impairs insulin signaling in obesity

Project description:Insulin resistance is the hallmark of obese and type 2 diabetes patients. Defective insulin sensitivity in the liver results in increased glucsoe production, which is the major cause of hyperglycemia in diabetic patients. Increased lipopolysaccharide (LPS) leakage from the gut of diet-induced obesity causes insulin resisitance; moreover, activation of deacetylase Sirtuin1 restore insulin sensitivity in obesity. However, the mechanism resulting in insulin resistance by LPS remains poorly understood. Here, we show that Ep300 (P300) harboring an intrinsic acetyltransferase activity was rapidly induced in the liver of animals fed a high-fat diet, and the induction of Ep300 is through LPS-stimulated activation of ER stress. Induced Ep300 impairs insulin signaling by acetylating mediators in insulin signaling. Inhibition of P300 acetyltransferase activity improves insulin signaling. Thus, Ep300 acetyltransferase activity is a therapeutic target.

2017-05-08 | GSE86108 | GEO

Genome-wide assessment of differential roles for p300 and CBP in transcription regulation

2010-03-30 | GSE21026 | GEO

Selective roles of p300 and CBP in androgen regulated gene expression

Project description:C4-2B prostate cancer cells were transfected with siRNA against a non-specific (NS) sequence, siRNA specifically targeting EP300, or siRNA specifically targeting CREBBP. We tested the hypothesis that their exists different subgroups of genes that are preferentially affected by p300 or CBP depletion. Cells were treated with 10nM dihydrotestosterone (DHT) for 16 hours and total RNA was extracted to check for changes in gene expression.

2011-12-15 | E-GEOD-31873 | biostudies-arrayexpress

Regulation of p300 acetyltransferase activity by the TAZ2 domain [RNA-seq]

Project description:The E1A binding protein P300 (EP300, also known as p300, lysine acetyltransferase 3B or KAT3B) and its close paralogue CREB-binding protein (CREBBP, aka CBP or KAT3A) possess intrinsic histone acetyltransferase (HAT) activity that can act on both histone and non-histone proteins. P300 and CBP are composed of multiple conserved protein domains, many of which are in proximity to the HAT domain modulating its catalytic activity. Here we show that the TAZ2 domain regulates the intrinsic catalytic activity of p300 in vitro and histone acetylation and chromatin accessibility in cells. Our study extends the knowledge of p300 self-regulation and provides new therapeutic stratagies for human cancers with corresponding p300/CBP mutations.

2023-08-07 | GSE193645 | GEO

Regulation of p300 acetyltransferase activity by the TAZ2 domain [ATAC-seq]

2023-08-07 | GSE193647 | GEO

Regulation of p300 acetyltransferase activity by the TAZ2 domain [ChIP-seq]

2023-08-07 | GSE193646 | GEO

Sodium arsenite exposure inhibits histone acetyltransferase p300 for attenuating H3K27ac at enhancers in mouse embryonic fibroblast cells

Project description:Both epidemiological investigations and animal studies have linked arsenic-contaminated water to cancers, in- cluding skin, liver and lung cancers. Besides genotoxicity, arsenic exposure-related pathogenesis of disease is widely considered through epigenetic mechanisms; however, the underlying mechanism remains to be deter- mined. Herein we explore the initial epigenetic changes via acute sodium arsenite (As) exposures of mouse em- bryonic fibroblast (MEF) cells and histone H3K79 methyltransferase Dot1L knockout (Dot1L−⁠ /−) MEF cells. Our RNA-seq and Western blot data demonstrated that, in both cell lines, acute As exposure abolished histone acetyl- transferase p300 at the RNA level and subsequent protein level. Consequently, p300-specific main target histone H3K27ac, a marker separating active from poised enhancers, decreased dramatically as validated by both West- ern blot and ChIP-qPCR/seq analyses. Concomitantly, H3K4me1 as another well-known marker for enhancers also showed significant decreases, suggesting an underappreciated crosstalk between H3K4me1 and H3K27ac involved in As exposure. Significantly, As exposure-reduced H3K27ac and H3K4me1 inhibited the expression of genes including EP300 itself and Kruppel Like Factor 4(Klf4) that both are tumor suppressor genes. Collectively, our investigations identified p300 as an internal bridging factor within cells to sense external environmental As exposure to alter chromatin, thereby changing gene transcription for disease pathogenesis.

2020-12-10 | GSE118827 | GEO

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