E-GEOD-46493
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA200647PRJNA201486PRJNA201484
PROVIDER: E-GEOD-46493 | ExpressionAtlas | 2015-07-13
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-46493-analysis-methods.tsv | Tabular | |||
| E-GEOD-46493-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-46493-configuration.xml | Xml | |||
| E-GEOD-46493-percentile-ranks.tsv | Tabular | |||
| E-GEOD-46493.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 71 |
Similar Datasets
Project description:Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells (Affymetrix)
| PRJNA200647 | ENA
Project description:Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells
| PRJNA201484 | ENA
Project description:Diverse stresses dramatically alter genome-wide p53 binding and transactivation landscape in human cancer cells (ChIP-seq)
| PRJNA201486 | ENA
Project description:We report here genome-wide analysis of the tumor suppressor p53 binding sites in normal human cells. 743 high-confidence ChIP-seq peaks representing putative genomic binding sites were identified in normal IMR90 fibroblasts using a reference chromatin sample. More than 40 % were located within 2 kb of a transcription start site (TSS), a distribution similar to that documented for individually studied functional p53 binding sites and to date not observed by previous genome-wide studies. Nearly half of the high-confidence binding sites in the IMR90 cells reside in CpG islands, in marked contrast to sites reported in cancer-derived cells. The distinct genomic features of the IMR90 binding sites do not reflect a distinct preference for specific sequences, since the de novo developed p53 motif based on our study is similar to those reported by genome-wide studies of cancer cells. More likely the different chromatin landscape in normal compared to cancer-derived cells influences p53 binding via modulating availability of the sites. We compared the IMR90 ChIP-seq peaks to the recently published IMR90 methylome1, and demonstrated that they are enriched at hypomethylated DNA. Our study represents the first genome-wide, de novo mapping of p53 binding sites in normal human cells and reveals that p53 binding sites reside in distinct genomic landscapes in normal and cancer-derived human cells. Identification of genomic p53 binding sites in normal human cells by ChIP-seq.
2011-12-08 | E-GEOD-31558 | biostudies-arrayexpress
Project description:We report here genome-wide analysis of the tumor suppressor p53 binding sites in normal human cells. 743 high-confidence ChIP-seq peaks representing putative genomic binding sites were identified in normal IMR90 fibroblasts using a reference chromatin sample. More than 40 % were located within 2 kb of a transcription start site (TSS), a distribution similar to that documented for individually studied functional p53 binding sites and to date not observed by previous genome-wide studies. Nearly half of the high-confidence binding sites in the IMR90 cells reside in CpG islands, in marked contrast to sites reported in cancer-derived cells. The distinct genomic features of the IMR90 binding sites do not reflect a distinct preference for specific sequences, since the de novo developed p53 motif based on our study is similar to those reported by genome-wide studies of cancer cells. More likely the different chromatin landscape in normal compared to cancer-derived cells influences p53 binding via modulating availability of the sites. We compared the IMR90 ChIP-seq peaks to the recently published IMR90 methylome1, and demonstrated that they are enriched at hypomethylated DNA. Our study represents the first genome-wide, de novo mapping of p53 binding sites in normal human cells and reveals that p53 binding sites reside in distinct genomic landscapes in normal and cancer-derived human cells.
2011-12-08 | GSE31558 | GEO
Project description:The effects of diverse stresses on promoter selectivity and transcription regulation by the tumor suppressor p53 are poorly understood. We have taken a comprehensive approach to characterizing the human p53 network that includes p53 levels, binding, expression and chromatin changes under diverse stresses. Human osteosarcoma U2OS cells treated with anti-cancer drugs Doxorubicin or Nutlin-3 led to strikingly different p53 gene binding patterns based on ChIP-seq experiments. While two contiguous RRRCWWGYYY decamers is the consensus binding motif, p53 can bind a single decamer and function in vivo. Although the number of sites bound by p53 was 6-times greater for Nutlin-3 than Doxorubicin, expression changes induced by Nutlin-3 were much less dramatic compared to Doxorubicin. Unexpectedly, the solvent DMSO alone induced p53 binding to many sites common to Doxorubicin; however, this binding had no effect on target gene expression. Together, these data imply a two-stage mechanism for p53 transactivation where p53 binding only constitutes the first stage. Furthermore, both p53 binding and transactivation were associated with increased active histone modification H3K4me3. We discovered 149 putative new p53 target genes including several that are relevant to tumor suppression, revealing potential new targets for cancer therapy and expanding our understanding of the p53 regulatory network. Gene expression analysis (using Affymetrix Human Genome U133 Plus 2.0 GeneChip® arrays) of the p53 response in U2OS cells treated with either Doxorubicin or Nutlin-3, relative to their controls No Treatment and DMSO, respectively.
2013-07-01 | E-GEOD-46493 | biostudies-arrayexpress
Project description:To determine if induced p53 binding is associated with gene expression in genome-wide. We examined mRNA levels with the Affymetrix Human Exon 1.0 ST platform in human lymphoblastoid GM12878 cells treated with doxorubicin to activate p53. In response to various cellular stresses, the tumor suppressor gene p53 induces activation or repression of more than a thousand human genes. Selective binding and transactivation of a large potential pool of p53 response elements (REs) is believed to regulate the variation in stress response across stress types and between cell types. To elucidate how the human genome is targeted by p53 at the chromatin level, we mapped the genome-wide localization of p53 and H3K4me3 from Doxo-treated human lymphoblastoid cells, and examined the relationships among p53 occupancy, gene expression, H3K4me3, chromatin accessibility (DNase 1 Hypersensitivity, DHS), ENCODE chromatin states, RE sequence specificity and evolutionary conservation.
2014-11-14 | GSE51709 | GEO
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
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.
2014-11-21 | GSE58714 | GEO
Project description:The tumor suppressor protein p53 functions to regulate diverse cellular processes including apoptosis, cell cycle, senescence and metabolism. Act as a master transcription factor, it can transcriptionally regulate the gene expression of many downstream target genes. p53 is frequently mutated in cancer by single nucleotide/amino acid substitutions at the DNA binding domain that result in a mutant form of p53 protein and usually loses its DNA binding and transcriptional regulation abilities. In this study, we performed gene expression analysis using Affymetrix Exon Array ST1.0 platform to assess the transcriptome of wildtype p53 and 6 loss-of-function p53 mutants in p53null HCT116 cells.
2013-08-19 | GSE49046 | GEO