Evidence map›Paper›PMID 21911363›Full record

ArticleNucleic acids research2012

Inhibition of p53 acetylation by INHAT subunit SET/TAF-Iβ represses p53 activity.

Ji-Young Kim, Kyu-Sun Lee, Jin-Ee Seol, Kweon Yu, Debabrata Chakravarti, Sang-Beom Seo

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. The oncoprotein SET promotes serine-derived one-carbon metabolism by regulating SHMT2 enzymatic activity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. The next decade of SET: from an oncoprotein to beyond.Journal of molecular cell biology · 2024
    Review
  8. Article
  9. Unusual Presentation ofInternational journal of molecular sciences · 2023
    Article
  10. The impact of SETBP1 mutations in neurological diseases and cancer.Genes to cells : devoted to molecular & cellular mechanisms · 2023
    Review
  11. Article
  12. The SET oncoprotein promotes estrogen-induced transcription by facilitating establishment of active chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 3 institutions in 2 countries.

Ji-Young KimDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 156-756, Korea.
Kyu-Sun Lee
Jin-Ee Seol
Kweon Yu
Debabrata Chakravarti
Sang-Beom Seo
Chung-Ang University · KRKorea Research Institute of Bioscience and Biotechnology · KRNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor p53 responds to a wide variety of cellular stress signals. Among potential regulatory pathways, post-translational modifications such as acetylation by CBP/p300 and PCAF have been suggested for modulation of p53 activity. However, exactly how p53 acetylation is modulated remains poorly understood. Here, we found that SET/TAF-Iβ inhibited p300- and PCAF-mediated p53 acetylation in an INHAT (inhibitor of histone acetyltransferase) domain-dependent manner. SET/TAF-Iβ interacted with p53 and repressed transcription of p53 target genes. Consequently, SET/TAF-Iβ blocked both p53-mediated cell cycle arrest and apoptosis in response to cellular stress. Using different apoptosis analyses, including FACS, TUNEL and BrdU incorporation assays, we also found that SET/TAF-Iβ induced cellular proliferation via inhibition of p53 acetylation. Furthermore, we observed that apoptotic Drosophila eye phenotype induced by either dp53 overexpression or UV irradiation was rescued by expression of dSet. Inhibition of dp53 acetylation by dSet was observed in both cases. Our findings provide new insights into the regulation of stress-induced p53 activation by HAT-inhibiting histone chaperone SET/TAF-Iβ.

Indexed as

AcetylationAnimalsApoptosisApoptosis Regulatory ProteinsCell LineDrosophila melanogasterDrosophila ProteinsProtein Interaction Domains and MotifsProtein SubunitsRepressor ProteinsStress, PhysiologicalTranscriptional ActivationTumor Suppressor Protein p53Ultraviolet RaysApoptosis Regulatory ProteinsDrosophila Proteinsp53 protein, DrosophilaProtein SubunitsRepressor ProteinsSet protein, DrosophilaTumor Suppressor Protein p53

Identifiers

PMID21911363
PMCPMC3245910
OpenAlexW2087646825

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.