Evidence map›Paper›PMID 19805293›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

CBP and p300 are cytoplasmic E4 polyubiquitin ligases for p53.

Dingding Shi, Marius S Pop, Roman Kulikov, Ian M Love, Andrew L Kung, Andrew Kung, Steven R Grossman

Erratum issuedAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
8.9field-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

83 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
  2. E3 ubiquitin ligase SKP2 limits autophagosome formation duringFrontiers in cellular and infection microbiology · 2026
    Article
  3. CBP/p300, a promising therapeutic target for prostate cancer.Journal of translational medicine · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. EP300 as a Molecular Integrator of Fibrotic Transcriptional Programs.International journal of molecular sciences · 2023
    Review
  11. Article
  12. C/EBPβ enhances immunosuppression activity of myeloid-derived suppressor cells by a P300-mediated acetylation modification.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020
    Review

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

4 · The record

Corrections and comments

  • Erratum issued
    Kung, Andrew [corrected to Kung, Andrew L]
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Dingding ShiDepartment of Cancer Biology, University of Massachusetts Medical School and University of Massachusetts Memorial Cancer Center, 364 Plantation Street, Worcester, MA 01605, USA.
Marius S Pop
Roman Kulikov
Ian M Love
Andrew L Kung
Andrew Kung
Steven R Grossman
Dana-Farber Cancer Institute · USUniversity of Massachusetts Chan Medical School · US

Funding

Role of p300/CBP and hHR23 Proteins in p53 RegulationR01CA107532 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GROSSMAN, STEVEN R. · 2004 to 2014
$2.6M
NCI NIH HHS R01 CA107532NCI NIH HHS R01CA107532
6 · The paper itself

Abstract

p300 and CREB-binding protein (CBP) act as multifunctional regulators of p53 via acetylase and polyubiquitin ligase (E4) activities. Prior work in vitro has shown that the N-terminal 595 aa of p300 encode both generic ubiquitin ligase (E3) and p53-directed E4 functions. Analysis of p300 or CBP-deficient cells revealed that both coactivators were required for endogenous p53 polyubiquitination and the normally rapid turnover of p53 in unstressed cells. Unexpectedly, p300/CBP ubiquitin ligase activities were absent in nuclear extracts and exclusively cytoplasmic. Consistent with the cytoplasmic localization of its E3/E4 activity, CBP deficiency specifically stabilized cytoplasmic, but not nuclear p53. The N-terminal 616 aa of CBP, which includes the conserved Zn(2+)-binding C/H1-TAZ1 domain, was the minimal domain sufficient to destabilize p53 in vivo, and it included within an intrinsic E3 autoubiquitination activity and, in a two-step E4 assay, exhibited robust E4 activity for p53. Cytoplasmic compartmentalization of p300/CBP's ubiquitination function reconciles seemingly opposed functions and explains how a futile cycle is avoided-cytoplasmic p300/CBP E4 activities ubiquitinate and destabilize p53, while physically separate nuclear p300/CBP activities, such as p53 acetylation, activate p53.

Indexed as

Cell Line, TumorCREB-Binding ProteinCytoplasmE1A-Associated p300 ProteinGene Expression Regulation, NeoplasticHumansImmunoblottingPolyubiquitinReverse Transcriptase Polymerase Chain ReactionTumor Suppressor Protein p53Tumor Suppressor ProteinsUbiquitin-Protein Ligase ComplexesUbiquitin-Protein LigasesCREB-Binding ProteinE1A-Associated p300 ProteinEP300 protein, humanPolyubiquitinTumor Suppressor Protein p53Tumor Suppressor ProteinsUBE4A protein, humanUBE4B protein, humanUbiquitin-Protein Ligase ComplexesUbiquitin-Protein Ligases

Identifiers

PMID19805293
PMCPMC2752525
OpenAlexW2136882950

What OpenQuestion holds

Textmetadata
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.