ArticleOncotarget2012
Gain-of-function p53 mutants have widespread genomic locations partially overlapping with p63.
Article in Oncotarget, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 46 citations in OpenAlex.
- The p53-Associated Regulation of ATF4 mRNA Expression Involves p21 and p130 in a Stress-Dependent Manner.Cells · 2026Article
- Deficient arsenic methylation and global proteomic reprogramming in human keratinocytes during arsenic-induced skin carcinogenesis.Archives of toxicology · 2026Article
- Dysregulation of mRNA expression by hsa-miR-186 overexpression in arsenic-induced skin carcinogenesis.Toxicology and applied pharmacology · 2025Article
- Exploring the Functions of Mutant p53 throughCurrent issues in molecular biology · 2024Article
- The Status of p53 Oligomeric and Aggregation States in Cancer.Biomolecules · 2020Review
- Disruption of TP63-miR-27a* Feedback Loop by Mutant TP53 in Head and Neck Cancer.Journal of the National Cancer Institute · 2020Article
- Mutant p53 as a guardian of the cancer cell.Cell death and differentiation · 2019Review
- Differentially Expressed mRNA Targets of Differentially Expressed miRNAs Predict Changes in the TP53 Axis and Carcinogenesis-Related Pathways in Human Keratinocytes Chronically Exposed to Arsenic.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Complexes formed by mutant p53 and their roles in breast cancer.Breast cancer (Dove Medical Press) · 2018Review
- Proteasome machinery is instrumental in a common gain-of-function program of the p53 missense mutants in cancer.Nature cell biology · 2016Article
- p63/MT1-MMP axis is required for in situ to invasive transition in basal-like breast cancer.Oncogene · 2016Article
- ΔNp63α Transcriptionally Regulates the Expression of CTEN That Is Associated with Prostate Cell Adhesion.PloS one · 2016Article
- Transcription factor p63 bookmarks and regulates dynamic enhancers during epidermal differentiation.EMBO reports · 2015Article
- HPV16 E5 deregulates the autophagic process in human keratinocytes.Oncotarget · 2015Article
- IFI27, a novel epidermal growth factor-stabilized protein, is functionally involved in proliferation and cell cycling of human epidermal keratinocytes.Cell proliferation · 2015Article
- Integrated transcriptional profiling and genomic analyses reveal RPN2 and HMGB1 as promising biomarkers in colorectal cancer.Cell & bioscience · 2015Article
- Review
- Unravelling mechanisms of p53-mediated tumour suppression.Nature reviews. Cancer · 2014Article
- Preferred binding of gain-of-function mutant p53 to bidirectional promoters with coordinated binding of ETS1 and GABPA to multiple binding sites.Oncotarget · 2014Article
- 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
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 and p63 are transcription factors -TFs- playing master roles in the DNA-damage response and in the development and maintenance of pluristratified epithelia, respectively. p53 mutations are common in epithelial tumors and HaCaT keratinocytes harbor two p53 alleles -H179Y and R282Q- with gain-of-function (GOF) activity. Indeed, functional inactivation of mutp53 affects the growth rate of HaCaT. We investigated the strategy of mutp53, by performing ChIP-Seq experiments of mutp53 and p63 and analyzed the transcriptome after mutp53 inactivation. Mutp53 bind to 7135 locations in vivo, with a robust overlap with p63. De novo motifs discovery recovered a p53/p63RE with high information content in sites bound by p63 and mutp53/p63, but not by mutp53 alone: these sites are rather enriched in elements of other TFs. The HaCaT p63 locations are only partially overlapping with those of normal keratinocytes; importantly, and enriched in mutp53 sites which delineate a functionally different group of target genes. Our data favour a model whereby mutp53 GOF mutants act both by tethering growth-controlling TFs and highjacking p63 to new locations.
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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.