Evidence map›Paper›PMID 35487975›Full record

ReviewOncogene2022

Deciphering the acetylation code of p53 in transcription regulation and tumor suppression.

Zhangchuan Xia, Ning Kon, Alyssa P Gu, Omid Tavana, Wei Gu

Open access · greenAbstract readReview
In one paragraph

Review in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. The Role of P53 in Myocardial Ischemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2025
    Review
  20. p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Zhangchuan XiaInstitute for Cancer Genetics, and Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY, 10032, USA.
Ning KonInstitute for Cancer Genetics, and Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY, 10032, USA.
Alyssa P GuInstitute for Cancer Genetics, and Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY, 10032, USA.
Omid TavanaInstitute for Cancer Genetics, and Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY, 10032, USA.
Wei GuInstitute for Cancer Genetics, and Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY, 10032, USA. wg8@cumc.columbia.edu.ORCID http://orcid.org/0000-0002-1480-2368
Cancer Genetics (United States) · USColumbia University · US

Funding

p53-mediated metabolic regulation in tumor suppressionR35CA253059 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Wei Gu · 2021 to 2026
$5.3M
Co-regulation of p53 and PD-L1 by the VPRBP-USP2 axis in transcription and ubiquitylationR01CA258390 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Wei Gu · 2022 to 2026
$2.3M
Novel small molecule USP7 Inhibitors for p53 activation and cancer therapyR01CA254970 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2021 to 2025
$1.8M
NCI NIH HHS R01 CA254970NCI NIH HHS R01 CA258390NCI NIH HHS R35 CA253059
6 · The paper itself

Abstract

Although it is well-established that p53-mediated tumor suppression mainly acts through its ability in transcriptional regulation, the molecular mechanisms of this regulation are not completely understood. Among a number of regulatory modes, acetylation of p53 attracts great interests. p53 was one of the first non-histone proteins found to be functionally regulated by acetylation and deacetylation, and subsequent work has established that reversible acetylation is a general mechanism for regulation of non-histone proteins. Unlike other types of posttranslational modifications occurred during stress responses, the role of p53 acetylation has been recently validated in vivo by using the knock-in mice with both acetylation-defective and acetylation-mimicking p53 mutants. Here, we review the role of acetylation in p53-mediated activities, with a focus on which specific acetylation sites are critical for p53-dependent transcription regulation during tumor suppression and how acetylation of p53 recruits specific "readers" to execute its promoter-specific regulation of different targets. We also discuss the role of p53 acetylation in differentially regulating its classic activities in cell cycle arrest, senescence and apoptosis as well as newly identified unconventional functions such as cell metabolism and ferroptosis.

Indexed as

NeoplasmsAcetylationAnimalsApoptosisCell Cycle CheckpointsHumansMiceProtein Processing, Post-TranslationalTumor Suppressor Protein p53Trp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID35487975
PMCPMC9149126
OpenAlexW4225101492

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.