ArticlePLoS genetics2015
Phenotype specific analyses reveal distinct regulatory mechanism for chronically activated p53.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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
40 citing papers in PubMed, 64 citations in OpenAlex.
- p53 status determines the epigenetic response to demethylating agents azacitidine and decitabine.EMBO reports · 2026Article
- Effects of Chlorogenic Acid on Cellular Senescence in an In Vitro Model of 3T3-L1 Murine Adipocytes.Molecules (Basel, Switzerland) · 2026Article
- p53 inactivation drives breast cancer metastasis to the brain through SCD1 upregulation and increased fatty acid metabolism.Nature genetics · 2026Article
- Cellular senescence in cancer immunology and potential therapeutic strategy.Frontiers in oncology · 2026Review
- Treating Metabolic Dysregulation and Senescence by Caloric Restriction: Killing Two Birds with One Stone?Antioxidants (Basel, Switzerland) · 2025Review
- Skeletal muscle p53-depletion uncovers a mechanism of fuel usage suppression that enables efficient energy conservation.Journal of cachexia, sarcopenia and muscle · 2024Article
- p53 target ANKRA2 cooperates with RFX7 to regulate tumor suppressor genes.Cell death discovery · 2024Article
- HMGA1 orchestrates chromatin compartmentalization and sequesters genes into 3D networks coordinating senescence heterogeneity.Nature communications · 2024Article
- Systematic transcriptomic analysis and temporal modelling of human fibroblast senescence.Frontiers in aging · 2024Article
- Metabolic Interplay in the Tumor Microenvironment: Implications for Immune Function and Anticancer Response.Current issues in molecular biology · 2023Review
- The impact of cellular senescence in human adipose tissue.Journal of cell communication and signaling · 2023Review
- Regulation of VKORC1L1 is critical for p53-mediated tumor suppression through vitamin K metabolism.Cell metabolism · 2023Article
- Unveiling the MUFA-Cancer Connection: Insights from Endogenous and Exogenous Perspectives.International journal of molecular sciences · 2023Review
- Nucleoplasmic lamin C rapidly accumulates at sites of nuclear envelope rupture with BAF and cGAS.The Journal of cell biology · 2022Article
- Integrated multi-omics approach revealed cellular senescence landscape.Nucleic acids research · 2022Article
- Article
- Locus-specific induction of gene expression from heterochromatin loci during cellular senescence.Nature aging · 2022Article
- The multifunctional protein E4F1 links P53 to lipid metabolism in adipocytes.Nature communications · 2021Article
- p53-Dependent Repression: DREAM or Reality?Cancers · 2021Article
- Cellular senescence in ageing: from mechanisms to therapeutic opportunities.Nature reviews. Molecular cell biology · 2021Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
Abstract
The downstream functions of the DNA binding tumor suppressor p53 vary depending on the cellular context, and persistent p53 activation has recently been implicated in tumor suppression and senescence. However, genome-wide information about p53-target gene regulation has been derived mostly from acute genotoxic conditions. Using ChIP-seq and expression data, we have found distinct p53 binding profiles between acutely activated (through DNA damage) and chronically activated (in senescent or pro-apoptotic conditions) p53. Compared to the classical 'acute' p53 binding profile, 'chronic' p53 peaks were closely associated with CpG-islands. Furthermore, the chronic CpG-island binding of p53 conferred distinct expression patterns between senescent and pro-apoptotic conditions. Using the p53 targets seen in the chronic conditions together with external high-throughput datasets, we have built p53 networks that revealed extensive self-regulatory 'p53 hubs' where p53 and many p53 targets can physically interact with each other. Integrating these results with public clinical datasets identified the cancer-associated lipogenic enzyme, SCD, which we found to be directly repressed by p53 through the CpG-island promoter, providing a mechanistic link between p53 and the 'lipogenic phenotype', a hallmark of cancer. Our data reveal distinct phenotype associations of chronic p53 targets that underlie specific gene regulatory mechanisms.
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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.