Evidence map›Paper›PMID 20932800›Full record

ReviewTrends in molecular medicine2010

p53 post-translational modification: deregulated in tumorigenesis.

Chao Dai, Wei Gu

Open access · greenAbstract readReview
In one paragraph

Review in Trends in molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 307 papers.

0numbers the graph read from it
0cells of the map it votes in
307citing papers in PubMed
16.7field-weighted citation impact, top 1% 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

307 citing papers in PubMed, 526 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Delving Into the Depths ofHuman mutation · 2026
    Article
  8. Article
  9. TheiScience · 2025
    Article
  10. Preclinical Modeling of Navtemadlin Pharmacokinetics, Pharmacodynamics, and Efficacy in IDH-Wild-type Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025
    Review
  20. Article

247 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Chao DaiInstitute for Cancer Genetics, College of Physicians and Surgeons, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA.
Wei Gu
Cancer Genetics (United States) · USColumbia University · US

Funding

PW1--A mediator of cell survival by NFKB and cell death by p53P01CA080058 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI AARONSON, STUART A · 2000 to 2016
$20.2M
The role of PTEN in basal-like breast cancerP01CA097403 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PARSONS, RAMON E · 2003 to 2013
$18.2M
Regulation of p53 acetylation and deacetylation in tumorigenesis.R01CA085533 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2000 to 2021
$5.2M
Mechanisms of Mdm2/Mdmx in repressing p53R01CA131439 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2009 to 2013
$1.6M
Dynamic roles of HAUSP in p53/Mdm2 regulationR01CA129627 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2007 to 2011
$1.5M
The role of ARF-BP1 in tumorigenesisR01CA118561 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2006 to 2010
$1.2M
NCI NIH HHS P01 CA080058NCI NIH HHS P01 CA097403NCI NIH HHS R01 CA085533NCI NIH HHS R01 CA118561NCI NIH HHS R01 CA129627NCI NIH HHS R01 CA131439
6 · The paper itself

Abstract

The p53 tumor suppressor protein has well-established roles in monitoring various types of stress signals by activating specific transcriptional targets that control cell cycle arrest and apoptosis, although some activities are also mediated in a transcription-independent manner. Here, we review the recent advances in our understanding of the wide spectrum of post-translational modifications that act as epigenetic-like codes for modulating specific functions of p53 in vivo and how deregulation of these modifications might contribute to tumorigenesis. We also discuss future research priorities to further understand p53 post-translational modifications and the interpretation of genetic data in appreciation of the increasing evidence that p53 regulates cellular metabolism, autophagy and many unconventional tumor suppressor activities.

Indexed as

Protein Processing, Post-TranslationalAcetylationAnimalsGene Expression Regulation, NeoplasticHumansMethylationNeoplasmsPhosphorylationTumor Suppressor Protein p53UbiquitinationTumor Suppressor Protein p53

Identifiers

PMID20932800
PMCPMC2978905
OpenAlexW2010706742

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.