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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Peter 't Hoen

PROVIDER: E-GEOD-21026 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Ramos Yolande F M YF Hestand Matthew S MS Verlaan Matty M Krabbendam Elise E Ariyurek Yavuz Y van Galen Michiel M van Dam Hans H van Ommen Gert-Jan B GJ den Dunnen Johan T JT Zantema Alt A 't Hoen Peter A C PA

Nucleic acids research 20100430 16

Despite high levels of homology, transcription coactivators p300 and CREB binding protein (CBP) are both indispensable during embryogenesis. They are largely known to regulate the same genes. To identify genes preferentially regulated by p300 or CBP, we performed an extensive genome-wide survey using the ChIP-seq on cell-cycle synchronized cells. We found that 57% of the tags were within genes or proximal promoters, with an overall preference for binding to transcription start and end sites. The ...[more]

PMID: 20435671

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Expression data from wild type and CBP/p300 null MEFs +/- 3hr treatment with 100uM dipyridyl (DP)

Project description:Genome-wide distribution of histone H3K18 and H3K27 acetyltransferases, Crebbp (CBP) and Ep300 (p300), is used to map enhancers and promoters, but whether these elements functionally require CBP/p300 remains largely uncertain. We investigated this relationship by comparing genomic CBP recruitment with gene expression in wild type and CBP/p300 double-knockout fibroblasts. ChIP-seq revealed nearby CBP recruitment for 20 percent of constitutively expressed genes, but surprisingly, three-quarters of these were unaffected or slightly activated by CBP/p300 deletion. Computationally defined enhancer-promoter-units (EPUs) having a CBP peak within two kilobases of the enhancer-like element provided better predictive value, with CBP/p300 deletion attenuating expression of 40 percent of such EPU assigned constitutively expressed genes. We next examined signaling-responsive (Hypoxia Inducible Factor) gene expression and CBP recruitment, and found that 97 percent of inducible genes were within 50 kilobases of an inducible CBP peak, and 70 percent of these required CBP/p300 for full inducible expression. Unexpectedly however, most inducible CBP peaks occurred near signal-nonresponsive genes. 12 samples, 3 each wild type and CBP/p300 null treated for 3hrs with 100uM dipyridyl orethanol vehicle.

2014-09-29 | E-GEOD-54452 | biostudies-arrayexpress

CREBBP (CBP) ChIP-seq in wild type and CBP null MEFs +/- dipyridyl

Project description:Genome-wide distribution of histone H3K18 and H3K27 acetyltransferases, Crebbp (CBP) and Ep300 (p300), is used to map enhancers and promoters, but whether these elements functionally require CBP/p300 remains largely uncertain. We investigated this relationship by comparing genomic CBP recruitment with gene expression in wild type and CBP/p300 double-knockout fibroblasts. ChIP-seq revealed nearby CBP recruitment for 20 percent of constitutively expressed genes, but surprisingly, three-quarters of these were unaffected or slightly activated by CBP/p300 deletion. Computationally defined enhancer-promoter-units (EPUs) having a CBP peak within two kilobases of the enhancer-like element provided better predictive value, with CBP/p300 deletion attenuating expression of 40 percent of such EPU assigned constitutively expressed genes. We next examined signaling-responsive (Hypoxia Inducible Factor) gene expression and CBP recruitment, and found that 97 percent of inducible genes were within 50 kilobases of an inducible CBP peak, and 70 percent of these required CBP/p300 for full inducible expression. Unexpectedly however, most inducible CBP peaks occurred near signal-nonresponsive genes. eight samples total; Two wild type and two CBP null primary mouse embryonic fibroblast (MEF) lines, each treated with 100uM 2,2-dipyridyl or ethanol vehicle for 2 hours

2014-09-29 | E-GEOD-54453 | biostudies-arrayexpress

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.

2010-03-30 | GSE21026 | GEO

p300 and CBP are essential for skeletal muscle homeostasis, contractile function and survival

Project description:Reversible epsilon-amino acetylation of lysine residues regulates transcription as well as metabolic flux; however, roles for specific lysine acetyltransferases in skeletal muscle physiology and function remain enigmatic. In this study, we investigated the role of the homologous acetyltransferases p300 and CBP in skeletal muscle transcriptional homeostasis and physiology in adult mice. Mice with skeletal muscle-specific and inducible knockout of p300 and/or CBP were generated by crossing mice with a tamoxifen-inducible Cre recombinase expressed under the human alpha-skeletal actin (HSA) promoter with mice harboring LoxP sites flanking exon 9 of both the Ep300 and Crebbp genes. Knockout was induced at 13-15 weeks of age via oral gavage of tamoxifen. We demonstrate that loss of both p300 and CBP in adult mouse skeletal muscle severely impairs contractile function and results in lethality within one week – a phenotype that is reversed by the presence of a single allele of either p300 or CBP. The loss of muscle function in p300/CBP double knockout mice is paralleled by substantial transcriptional alterations in gene networks central to skeletal muscle contraction and structural integrity. Changes in protein expression patterns, determined by 10-plex TMT labeling, were linked to impaired muscle function also manifest within days (WT mice were compared to day 3 and day 5 knock out mice). Together, these data reveal the requirement of p300 and CBP for the control and maintenance of contractile function and transcriptional homeostasis in skeletal muscle, and ultimately, organism survival. By extension, modulating p300/CBP function holds promise for the treatment of disorders characterized by impaired contractile function in humans.

2020-04-03 | PXD015694 | Pride

Expression data from wild type and CBP/p300 null MEFs +/- 3hr treatment with 100uM dipyridyl (DP)

2014-09-29 | GSE54452 | GEO

CREBBP (CBP) ChIP-seq in wild type and CBP null MEFs +/- dipyridyl

2014-09-29 | GSE54453 | GEO

Regulation of p300 acetyltransferase activity by the TAZ2 domain [ATAC-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 | GSE193647 | GEO

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

2023-08-07 | GSE193646 | GEO

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

2023-08-07 | GSE193645 | GEO

RNA-seq of murine small intestinal organoids treated with Ep300/Crebbp inhibitor I-CBP112 against untreated controls

Project description:Murine small intestinal organoids were cultured in the presence or absence of 3µM inhibitor I-CBP112 (PubChem CID 90488984), which targets E1A Binding Protein P300 (Ep300) and Creb-binding protein (Crebbp, Cbp). Organoids were grown in culture media containing EGF, Noggin and R-spondin (ENR), media was changed after 48h, and organoids were harvested after 96h.

2020-12-16 | E-MTAB-9290 | biostudies-arrayexpress

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