ArticleCell cycle (Georgetown, Tex.)2012
The histone acetyltransferase PCAF regulates p21 transcription through stress-induced acetylation of histone H3.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 84 citations in OpenAlex.
- Acetylation-Mediated Epigenetic Consequences for Biological Control and Cancer.Results and problems in cell differentiation · 2025Review
- H3K14: A histone site closely related to diseases.Journal of Cancer · 2025Review
- Epigenetic Regulation in Myocardial Fibroblasts and Its Impact on Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Functional Investigations of p53 Acetylation Enabled by Heterobifunctional Molecules.ACS chemical biology · 2024Article
- PCAF promotes R-loop resolution via histone acetylation.Nucleic acids research · 2024Article
- Neuroinflammation and the role of epigenetic-based therapies for Huntington's disease management: the new paradigm.Inflammopharmacology · 2024Review
- Enhanced Transcriptional Signature and Expression of Histone-Modifying Enzymes in Salivary Gland Tumors.Cells · 2023Article
- Metformin Induces Apoptosis in Human Pancreatic Cancer (PC) Cells Accompanied by Changes in the Levels of Histone Acetyltransferases (Particularly, p300/CBP-Associated Factor (PCAF) Protein Levels).Pharmaceuticals (Basel, Switzerland) · 2023Article
- Acetylation State of Lysine 14 of Histone H3.3 Affects Mutant Huntingtin Induced Pathogenesis.International journal of molecular sciences · 2022Article
- Distinct p53 isoforms code for opposing transcriptional outcomes.Developmental cell · 2022Article
- The role of epigenetic modifications in Colorectal Cancer Metastasis.Clinical & experimental metastasis · 2022Review
- PCAF Accelerates Vascular Senescence via the Hippo Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- Nuclear myosin 1 activates p21 gene transcription in response to DNA damage through a chromatin-based mechanism.Communications biology · 2020Article
- Integrated Analysis of the Functions and Prognostic Values of RNA-Binding Proteins in Colorectal Cancer.Frontiers in cell and developmental biology · 2020Article
- Lysine Acetyltransferase Inhibitors From Natural Sources.Frontiers in pharmacology · 2020Review
- Epigenetic Regulation of p21Cancers · 2019Review
- Epigenetically Down-Regulated Acetyltransferase PCAF Increases the Resistance of Colorectal Cancer to 5-Fluorouracil.Neoplasia (New York, N.Y.) · 2019Article
- Bi-modal reprogramming of cell cycle by MiRNA-4673 amplifies human neurogenic capacity.Cell cycle (Georgetown, Tex.) · 2019Article
- p300/CBP-associated factor promotes autophagic degradation of δ-catenin through acetylation and decreases prostate cancer tumorigenicity.Scientific reports · 2019Article
- ALT cancer cells are specifically sensitive to lysine acetyl transferase inhibition.Oncotarget · 2019Article
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5 authors at 2 institutions in 1 country.
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Abstract
The activity of p53 as a tumor suppressor primarily depends on its ability to transactivate specific target genes in response to genotoxic and other potentially mutagenic stresses. Several histone acetyl transferases (HATs), including p300, CBP, PCAF and GCN5 have been implicated in the activation of p53-dependent transcription of the cyclin-dependent kinase (cdk) inhibitor p21 as well as other target genes. Here we show that PCAF, but not CBP or p300, is a critical regulator of p53-dependent p21 expression in response to multiple p53-activating stresses. PCAF was required for the transcriptional activation of p21 in response to exogenous p53 in p53-null cells, nutlin-3, DNA damaging agents and p14(ARF) expression, suggesting a broad requirement for PCAF in p53 signaling to p21 after stress. Importantly, cells lacking PCAF failed to undergo cell cycle arrest in response to nutlin-3 treatment or p14(ARF) expression, consistent with a physiologically important role for PCAF in this p53 function. Surprisingly, the role for PCAF in induction of p21 was independent of p53 lysine 320 acetylation, a previously suggested target of PCAF-mediated acetylation. Though p21 promoter occupancy by p53 was not altered by PCAF knockdown, activation of p21 transcription required an intact PCAF HAT domain, and induction of chromatin marks acetyl-H3K9 and acetyl-H3K14 at the p21 promoter by p53 was dependent upon physiologic levels of PCAF. Together, our experiments indicate that PCAF is required for stress-responsive histone 3 acetylation at the p21 promoter, p53-directed transcription of p21 and the resultant growth arrest.
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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.