ArticlePloS one2014
Cell context dependent p53 genome-wide binding patterns and enrichment at repeats.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Integrative bioinformatic analysis of p53 and pathway alterations in two different lung cancer subtypes.Biochemistry and biophysics reports · 2023Article
- Differential p53-Mediated Cellular Responses to DNA-Damaging Therapeutic Agents.International journal of molecular sciences · 2021Review
- Article
- p53-Dependent Repression: DREAM or Reality?Cancers · 2021Article
- Temporal gene regulation by p53 is associated with the rotational setting of its binding sites in nucleosomes.Cell cycle (Georgetown, Tex.) · 2021Article
- Endogenous Retroviral-K Envelope Is a Novel Tumor Antigen and Prognostic Indicator of Renal Cell Carcinoma.Frontiers in oncology · 2021Article
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
- Article
- Transposons, p53 and Genome Security.Trends in genetics : TIG · 2018Review
- Revealing a human p53 universe.Nucleic acids research · 2018Article
- p53 positively regulates the expression of cancer stem cell marker CD133 in HCT116 colon cancer cells.Oncology letters · 2018Article
- Loss of p53-inducible long non-coding RNAOncotarget · 2017Article
- Germline TP53 mutations result into a constitutive defect of p53 DNA binding and transcriptional response to DNA damage.Human molecular genetics · 2017Article
- p53: Multiple Facets of a Rubik's Cube.Annual review of cancer biology · 2017Article
- Identification and Analysis of P53-Mediated Competing Endogenous RNA Network in Human Hepatocellular Carcinoma.International journal of biological sciences · 2017Article
- p53 binding sites in normal and cancer cells are characterized by distinct chromatin context.Cell cycle (Georgetown, Tex.) · 2017Article
- Multiplex enhancer-reporter assays uncover unsophisticated TP53 enhancer logic.Genome research · 2016Article
- detectMITE: A novel approach to detect miniature inverted repeat transposable elements in genomes.Scientific reports · 2016Article
- High-Resolution 4C Reveals Rapid p53-Dependent Chromatin Reorganization of the CDKN1A Locus in Response to Stress.PloS one · 2016Article
- p53 binding to human genome: crowd control navigation in chromatin context.Frontiers in genetics · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 ability to elicit stress specific and cell type specific responses is well recognized, but how that specificity is established remains to be defined. Whether upon activation p53 binds to its genomic targets in a cell type and stress type dependent manner is still an open question. Here we show that the p53 binding to the human genome is selective and cell context-dependent. We mapped the genomic binding sites for the endogenous wild type p53 protein in the human cancer cell line HCT116 and compared them to those we previously determined in the normal cell line IMR90. We report distinct p53 genome-wide binding landscapes in two different cell lines, analyzed under the same treatment and experimental conditions, using the same ChIP-seq approach. This is evidence for cell context dependent p53 genomic binding. The observed differences affect the p53 binding sites distribution with respect to major genomic and epigenomic elements (promoter regions, CpG islands and repeats). We correlated the high-confidence p53 ChIP-seq peaks positions with the annotated human repeats (UCSC Human Genome Browser) and observed both common and cell line specific trends. In HCT116, the p53 binding was specifically enriched at LINE repeats, compared to IMR90 cells. The p53 genome-wide binding patterns in HCT116 and IMR90 likely reflect the different epigenetic landscapes in these two cell lines, resulting from cancer-associated changes (accumulated in HCT116) superimposed on tissue specific differences (HCT116 has epithelial, while IMR90 has mesenchymal origin). Our data support the model for p53 binding to the human genome in a highly selective manner, mobilizing distinct sets of genes, contributing to distinct pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.