ArticleGenome research2015
TP53 engagement with the genome occurs in distinct local chromatin environments via pioneer factor activity.
Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
76 citing papers in PubMed, 2 syntheses or guidelines pooled it, 130 citations in OpenAlex.
- Genomic meta-analysis of the interplay between 3D chromatin organization and gene expression programs under basal and stress conditions.Epigenetics & chromatin · 2018Pooled it
- Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.Nucleic acids research · 2016Pooled it
- Targeted citrullination enables p53 binding to non-canonical sites.Molecular cell · 2025Article
- Iterative deep learning design of human enhancers exploits condensed sequence grammar to achieve cell-type specificity.Cell systems · 2025Article
- p53 reveals principles of chromatin remodeling and enhancer activation.Nucleic acids research · 2025Article
- Charting the regulatory landscape of TP53 on transposable elements in cancer.Genome research · 2025Article
- Nucleosome binding by TP53, TP63, and TP73 is determined by the composition, accessibility, and helical orientation of their binding sites.Genome research · 2025Article
- iModEst: disentangling -omic impacts on gene expression variation across genes and tissues.NAR genomics and bioinformatics · 2025Article
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025Article
- Decoding stimulus-specific regulation of promoter activity of p53 target genes.Frontiers in cell and developmental biology · 2025Article
- Determinants of p53 DNA binding, gene regulation, and cell fate decisions.Cell death and differentiation · 2024Review
- Chromatin organization drives the search mechanism of nuclear factors.Nature communications · 2023Article
- Transposable elements as tissue-specific enhancers in cancers of endodermal lineage.Nature communications · 2023Article
- Chromatin structure related to oncogenesis.Cancer science · 2023Review
- Integrative Identification by Hi-C Revealed Distinct Advanced Structural Variations in Lung Adenocarcinoma Tissue.Phenomics (Cham, Switzerland) · 2023Article
- Readout of histone methylation by Trim24 locally restricts chromatin opening by p53.Nature structural & molecular biology · 2023Article
- Decoding the lncRNAome Across Diverse Cellular Stresses Reveals Core p53-effector Pan-cancer Suppressive lncRNAs.Cancer research communications · 2023Article
- Histopathological and epigenetic changes in myocardium associated with cancer therapy-related cardiac dysfunction.ESC heart failure · 2022Article
- Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Despite overwhelming evidence that transcriptional activation by TP53 is critical for its tumor suppressive activity, the mechanisms by which TP53 engages the genome in the context of chromatin to activate transcription are not well understood. Using a compendium of novel and existing genome-wide data sets, we examined the relationship between TP53 binding and the dynamics of the local chromatin environment. Our analysis revealed three distinct categories of TP53 binding events that differ based on the dynamics of the local chromatin environment. The first class of TP53 binding events occurs near transcriptional start sites (TSS) and is defined by previously characterized promoter-associated chromatin modifications. The second class comprises a large cohort of preestablished, promoter-distal enhancer elements that demonstrates dynamic histone acetylation and transcription upon TP53 binding. The third class of TP53 binding sites is devoid of classic chromatin modifications and, remarkably, fall within regions of inaccessible chromatin, suggesting that TP53 has intrinsic pioneer factor activity and binds within structurally inaccessible regions of chromatin. Intriguingly, these inaccessible TP53 binding sites feature several enhancer-like properties in cell types within the epithelial lineage, indicating that TP53 binding events include a group of "proto-enhancers" that become active enhancers given the appropriate cellular context. These data indicate that TP53, along with TP63, may act as pioneer factors to specify epithelial enhancers. Further, these findings suggest that rather than following a global cell-type invariant stress response program, TP53 may tune its response based on the lineage-specific epigenomic landscape.
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Registered trials
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.