ArticleThe Journal of biological chemistry2009
p53 Oligomerization is essential for its C-terminal lysine acetylation.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 72 citations in OpenAlex.
- Revisiting the p53:Sirt1 interaction in light of controlling p53 acetylation levels.Communications chemistry · 2026Article
- p53 Interacts with VDAC1, Modulating Its Expression Level and Oligomeric State to Activate Apoptosis.Biomolecules · 2026Article
- Robust p53 phenotypes and prospective downstream targets in telomerase-immortalized human cells.Oncotarget · 2025Article
- Correlation of p53 oligomeric status and its subcellular localization in the presence of the AML-associated NPM mutant.PloS one · 2025Article
- Expanding the Substrate Scope of a Bacterial Nucleotidyltransferase via Allosteric Mutations.ACS infectious diseases · 2022Article
- Different Oligomeric States of the Tumor Suppressor p53 Show Identical Binding Behavior towards the S100β Homodimer.Chembiochem : a European journal of chemical biology · 2022Article
- Therapeutics Targeting p53-MDM2 Interaction to Induce Cancer Cell Death.International journal of molecular sciences · 2022Review
- Post-translational Modifications of the p53 Protein and the Impact in Alzheimer's Disease: A Review of the Literature.Frontiers in aging neuroscience · 2022Review
- Protein of a thousand faces: The tumor-suppressive and oncogenic responses of p53.Frontiers in molecular biosciences · 2022Review
- Tumor suppressor p53: Biology, signaling pathways, and therapeutic targeting.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- Review
- Semisynthetic 'designer' p53 sheds light on a phosphorylation-acetylation relay.Chemical science · 2021Article
- p53 tetramerization: at the center of the dominant-negative effect of mutant p53.Genes & development · 2020Review
- IDDomainSpotter: Compositional bias reveals domains in long disordered protein regions-Insights from transcription factors.Protein science : a publication of the Protein Society · 2020Article
- Regulation of the MDM2-p53 pathway by the ubiquitin ligase HERC2.Molecular oncology · 2020Article
- A new technique for predicting intrinsically disordered regions based on average distance map constructed with inter-residue average distance statistics.BMC structural biology · 2019Article
- Article
- Wild-type and cancer-related p53 proteins are preferentially degraded by MDM2 as dimers rather than tetramers.Genes & development · 2018Article
- A new era of studying p53-mediated transcription activation.Transcription · 2018Article
- Therapeutic targeting of p53: all mutants are equal, but some mutants are more equal than others.Nature reviews. Clinical oncology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Acetylation of multiple lysine residues in the p53 plays critical roles in the protein stability and transcriptional activity of p53. To better understand how p53 acetylation is regulated, we generated a number of p53 mutants and examined acetylation of each mutant in transfected cells. We found that p53 mutants that are defective in tetramer formation are also defective in C-terminal lysine residue acetylation. Consistently, we found that several cancer-derived p53 mutants that bear mutations in the tetramerization domain cannot form oligomers and are defective in C-terminal lysine acetylation, and these mutants are inactive in p21 transactivation. We demonstrated that the acetyltransferase p300 interacts with and promotes acetylation of wild-type p53 but not with any of the artificially generated or human cancer-derived p53 mutants that are defective in oligomerization. These results, combined with a computer-aided crystal structure analysis, suggest a model in which p53 oligomerization precedes its acetylation by providing docking sites for acetyltransferases.
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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.