ArticleProceedings of the National Academy of Sciences of the United States of America2013
MOZ increases p53 acetylation and premature senescence through its complex formation with PML.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed.
- Biological Activity and Structural Biology of Current KAT6A Inhibitor Chemotypes.Journal of medicinal chemistry · 2026Article
- Acetylation modification in malignant progression and therapeutic resistance of gliomas.Frontiers in cell and developmental biology · 2026Review
- Targeting lysine acetyltransferase 6A/B in cancer: a conceptual and translational review of epigenetic regulation, immune microenvironment remodeling, and the dual-compartment hypothesis.Frontiers in immunology · 2026Review
- Exploring KAT6 as a therapeutic target in breast cancer: epigenetic approaches for precision medicine.NPJ breast cancer · 2025Review
- T cell KAT6A deficiency relieves inflammatory bowel disease in mice.Cell & bioscience · 2025Article
- Heme drives cardiac endothelial senescence in sepsis via STING activation.Cell death & disease · 2025Article
- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025Review
- Translationally Controlled Tumor Protein (TCTP) and Growth Regulation in the Drosophila Model.Advances in experimental medicine and biology · 2025Article
- The advances in acetylation modification in senescence and aging-related diseases.Frontiers in physiology · 2025Review
- PML Nuclear bodies: the cancer connection and beyond.Nucleus (Austin, Tex.) · 2024Review
- Functional Investigations of p53 Acetylation Enabled by Heterobifunctional Molecules.ACS chemical biology · 2024Article
- KAT6A Condensates Impair PARP1 Trapping of PARP Inhibitors in Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- KAT6A/YAP/TEAD4 pathway modulates osteoclastogenesis by regulating the RANKL/OPG ratio on the compression side during orthodontic tooth movement.Progress in orthodontics · 2024Article
- A deep learning model of tumor cell architecture elucidates response and resistance to CDK4/6 inhibitors.Nature cancer · 2024Article
- Acetyltransferase in cardiovascular disease and aging.The journal of cardiovascular aging · 2024Article
- The postbiotic sodium butyrate synergizes the antiproliferative effects of dexamethasone against the AGS gastric adenocarcinoma cells.Frontiers in nutrition · 2024Article
- On the Prevalence and Roles of Proteins Undergoing Liquid-Liquid Phase Separation in the Biogenesis of PML-Bodies.Biomolecules · 2023Article
- KAT6A mutations in Arboleda-Tham syndrome drive epigenetic regulation of posterior HOXC cluster.Human genetics · 2023Article
42 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
Monocytic leukemia zinc finger (MOZ)/KAT6A is a MOZ, Ybf2/Sas3, Sas2, Tip60 (MYST)-type histone acetyltransferase that functions as a coactivator for acute myeloid leukemia 1 protein (AML1)- and Ets family transcription factor PU.1-dependent transcription. We previously reported that MOZ directly interacts with p53 and is essential for p53-dependent selective regulation of p21 expression. We show here that MOZ is an acetyltransferase of p53 at K120 and K382 and colocalizes with p53 in promyelocytic leukemia (PML) nuclear bodies following cellular stress. The MOZ-PML-p53 interaction enhances MOZ-mediated acetylation of p53, and this ternary complex enhances p53-dependent p21 expression. Moreover, we identified an Akt/protein kinase B recognition sequence in the PML-binding domain of MOZ protein. Akt-mediated phosphorylation of MOZ at T369 has a negative effect on complex formation between PML and MOZ. As a result of PML-mediated suppression of Akt, the increased PML-MOZ interaction enhances p21 expression and induces p53-dependent premature senescence upon forced PML expression. Our research demonstrates that MOZ controls p53 acetylation and transcriptional activity via association with PML.
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