ReviewCancers2014
p53 Acetylation: Regulation and Consequences.
Review in Cancers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
202 citing papers in PubMed, 320 citations in OpenAlex.
- PTP4A2 promotes leukemogenesis through inhibiting the p53 tumor suppressor signaling pathway in leukemia-initiating cells.Blood advances · 2026Article
- Advances in Mechanism of Action and Efficacy of CBP/p300 Inhibitors in Different Subtypes of Breast Cancer.Molecules (Basel, Switzerland) · 2026Review
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- Nitration in cancer signaling.Redox biology · 2026Review
- The NanoBridge system for targeted post-translational modification of challenging proteins.bioRxiv : the preprint server for biology · 2026Article
- The disulfonic acid ANDS disrupts ANP32B-p53 interaction to suppress chronic myeloid leukemia.Nature communications · 2026Article
- A Modular Platform for Effector Discovery in Induced-Proximity Lysine Acetylation.bioRxiv : the preprint server for biology · 2026Article
- Non-hydrolyzable acetyllysine analogs to study protein acetylation in vitro and in cells.Nature communications · 2026Article
- Tandem Allosteric Effects of Reactant and Product that Promote Deacetylation Cycles in Sir2.Journal of chemical information and modeling · 2025Article
- Citrullination negatively regulates the functions of the p53 protein and opposes its ubiquitination and degradation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- HDACs and Their Inhibitors on Post-Translational Modifications: The Regulation of Cardiovascular Disease.Cells · 2025Review
- Epigenomic Modulators and Thyroid Hormone Receptor β Agonists: A New Paradigm for Tumor Suppression in Thyroid Cancer.Endocrinology · 2025Review
- Targeting p53-p21 signaling to enhance mesenchymal stem cell regenerative potential.Regenerative therapy · 2025Review
- Post-translational modifications of epigenetic modifier TIP60: their role in cellular functions and cancer.Epigenetics & chromatin · 2025Review
- Meningiomas in Rubinstein-Taybi syndrome: A case report and comprehensive review.Journal of neuropathology and experimental neurology · 2025Review
- Unraveling the mechanisms of glioblastoma's resistance: investigating the influence of tumor suppressor p53 and non-coding RNAs.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Review
- Cracking Lysine Crotonylation (Kcr): Enlightening a Promising Post-Translational Modification.Chembiochem : a European journal of chemical biology · 2025Review
- How does p53 work? Regulation by the intrinsically disordered domains.Trends in biochemical sciences · 2025Review
- Purple Corn Extract Prevents Doxo-Induced Cardiotoxicity by Counteracting AMPK Activation and p53 Acetylation in HL-1 and Primary Cardiomyocytes.Oxidative medicine and cellular longevity · 2025Article
142 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Post-translational modifications of p53 are critical in modulating its tumor suppressive functions. Ubiquitylation, for example, plays a major role in dictating p53 stability, subcellular localization and transcriptional vs. non-transcriptional activities. Less is known about p53 acetylation. It has been shown to govern p53 transcriptional activity, selection of growth inhibitory vs. apoptotic gene targets, and biological outcomes in response to diverse cellular insults. Yet recent in vivo evidence from mouse models questions the importance of p53 acetylation (at least at certain sites) as well as canonical p53 functions (cell cycle arrest, senescence and apoptosis) to tumor suppression. This review discusses the cumulative findings regarding p53 acetylation, with a focus on the acetyltransferases that modify p53 and the mechanisms regulating their activity. We also evaluate what is known regarding the influence of other post-translational modifications of p53 on its acetylation, and conclude with the current outlook on how p53 acetylation affects tumor suppression. Due to redundancies in p53 control and growing understanding that individual modifications largely fine-tune p53 activity rather than switch it on or off, many questions still remain about the physiological importance of p53 acetylation to its role in preventing cancer.
Identifiers
What OpenQuestion holds
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.