Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Stereotyped p53 binding tuned by chromatin accessibility

ABSTRACT: We accessed the cell type specificity of p53 by directly measuring DNA binding in twelve cell lines in response to ionizing radiation. We find that that vast majority of binding sites are occupied across all cells lines uniformly, in contrast to p53 regulated gene expression which shows great diversity in the same context. We further identify a subset of p53 binding sites that are more restricted, appearing in one or a few cell lines. We find that chromatin accessibility explains much of these differential binding events.

ORGANISM(S): Homo sapiens

PROVIDER: GSE100292 | GEO | 2018/06/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Homo sapiens

Project description:Coupling p53 binding and nucleosome occupancy measurements at p53 binding sites

| PRJNA129117 | ENA

Cell Context Dependent p53 Genome-Wide Binding Patterns and Enrichment at Repeats

Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin. Identification of genomic p53 binding sites in HCT116 cells by ChIP-seq.

2014-11-21 | E-GEOD-58714 | biostudies-arrayexpress

The histone lysine demethylase JMJD3/KDM6B is recruited to p53 bound promoters and enhancer elements in a p53 dependent manner

Project description:The JmjC domain containing protein JMJD3/KDM6B catalyses H3K27me3 and H3K27me2 demethylation. JMJD3 appears to be highly regulated at the transcriptional level and is upregulated in response to diverse stimuli such as differentiation inducers and stress signals. Accordingly, JMJD3 has been linked to the regulation of different biological processes such as differentiation of embryonic stem cells, inflammatory responses in macrophages, and induction of cellular senescence via regulation of the INK4A-ARF locus. Here we show here that JMJD3 interacts with the tumour suppressor protein p53. We find that the interaction is dependent on the p53 tetramerization domain. Following DNA damage, JMJD3 is transcriptionally upregulated and by performing genome-wide mapping of JMJD3, we demonstrate that it binds genes involved in basic cellular processes, as well as genes regulating cell cycle, response to stress and apoptosis. Moreover, we find that JMJD3 binding sites show significant overlap with p53 bound promoters and enhancer elements. The binding of JMJD3 to p53 target sites is increased in response to DNA damage, and we demonstrate that the recruitment of JMJD3 to these sites is dependent on p53 expression. Therefore, we propose a model in which JMJD3 is recruited to p53 responsive elements via its interaction with p53 and speculate that JMJD3 could act as a fail-safe mechanism to remove low levels of H3K27me3 and H3K27me2 to allow for efficient acetylation of H3K27. Examination of JMJD3 and p53 genome-wide binding in untreated BJ cells or cells exposed to DNA damage (IR, 10 Gy)

2014-06-11 | E-GEOD-55912 | biostudies-arrayexpress

Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with ionizing radiation

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated withionizing radiation ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with ionizing radiation or vehicle

2013-10-23 | E-GEOD-46993 | biostudies-arrayexpress

Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with nutlin-3

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a MDM2 inhibitor nutlin-3 ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with nutlin-3 or vehicle

2013-10-23 | E-GEOD-46992 | biostudies-arrayexpress

Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle

2013-10-23 | E-GEOD-46991 | biostudies-arrayexpress

Coupling p53 binding and nucleosome occupancy measurements at p53 binding sites

2010-08-09 | GSE22783 | GEO

Homo sapiens

Project description:Chromatin dynamics of p53 binding sites in IMR90

| PRJNA253315 | ENA

Cell Context Dependent p53 Genome-Wide Binding Patterns and Enrichment at Repeats

2014-11-21 | GSE58714 | GEO

Coupling p53 binding and nucleosome occupancy measurements at p53 binding sites

Project description:We were interested to explain why p53 binds some high affinity sites in contrast to other high affinity sites that are not bound by p53. p53 binding was measured using p53 ChIP-CHIP and in parallel nucleosome occupancy was measured on these same sites Comparison between p53 binding and nucleosome occupancy at p53 predicted binding sites ChIP-CHIP of p53 from MCF7EcoR under Basal conditions and MCF7EcoR treated with NCS (Activated) and Mononucleosomal extraction from MCF7sip53, MCF7EcoR under Basal conditions and MCF7EcoR treated with NCS (Activated) Expression analysis of MCF7sip53 and MCF7EcoR treated with NCS (Activated)

2010-08-09 | E-GEOD-22783 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data