Evidence map›Paper›PMID 16537920›Full record

ArticleMolecular and cellular biology2006

Acetylation of p53 at lysine 373/382 by the histone deacetylase inhibitor depsipeptide induces expression of p21(Waf1/Cip1).

Ying Zhao, Shaoli Lu, Lipeng Wu, Guolin Chai, Haiying Wang, Yingqi Chen, Jia Sun, Yu Yu, Wen Zhou, Quanhui Zheng and 3 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

142 citing papers in PubMed, 274 citations in OpenAlex.

  1. Trial
  2. Phase II study of vorinostat for treatment of relapsed or refractory indolent non-Hodgkin's lymphoma and mantle cell lymphoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2011
    Trial
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  6. Review
  7. Article
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  10. Review
  11. Article
  12. Epigenetics.Advances in experimental medicine and biology · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

82 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

13 authors at 2 institutions in 2 countries.

Ying ZhaoDepartment of Biochemistry and Molecular Biology, Peking University Health Science Center, #38 Xueyuan Road, Beijing 100083, China.
Shaoli Lu
Lipeng Wu
Guolin Chai
Haiying Wang
Yingqi Chen
Jia Sun
Yu Yu
Wen Zhou
Quanhui Zheng
Mian Wu
Gregory A Otterson
Wei-Guo Zhu
Peking University · CNThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Generally, histone deacetylase (HDAC) inhibitor-induced p21(Waf1/Cip1) expression is thought to be p53 independent. Here we found that an inhibitor of HDAC, depsipeptide (FR901228), but not trichostatin A (TSA), induces p21(Waf1/Cip1) expression through both p53 and Sp1/Sp3 pathways in A549 cells (which retain wild-type p53). This is demonstrated by measuring relative luciferase activities of p21 promoter constructs with p53 or Sp1 binding site mutagenesis and was further confirmed by transfection of wild-type p53 into H1299 cells (p53 null). That p53 was acetylated after depsipeptide treatment was tested by sequential immunoprecipitation/Western immunoblot analysis with anti-acetylated lysines and anti-p53 antibodies. The acetylated p53 has a longer half-life due to a significant decrease in p53 ubiquitination. Further study using site-specific antiacetyllysine antibodies and transfection of mutated p53 vectors (K319/K320/K321R mutated and K373R/K382R mutations) into H1299 cells revealed that depsipeptide specifically induces p53 acetylation at K373/K382, but not at K320. As assayed by coimmunoprecipitation, the K373/K382 acetylation is accompanied by a recruitment of p300, but neither CREB-binding protein (CBP) nor p300/CBP-associated factor (PCAF), to the p53 C terminus. Furthermore, activity associated with the binding of the acetylated p53 at K373/K382 to the p21 promoter as well as p21(Waf1/Cip1) expression is significantly increased after depsipeptide treatment, as tested by chromatin immunoprecipitations and Western blotting, respectively. In addition, p53 acetylation at K373/K382 is confirmed to be required for recruitment of p300 to the p21 promoter, and the depsipeptide-induced p53 acetylation at K373/K382 is unlikely to be dependent on p53 phosphorylation at Ser15, Ser20, and Ser392 sites. Our data suggest that p53 acetylation at K373/K382 plays an important role in depsipeptide-induced p21(Waf1/Cip1) expression.

Indexed as

Histone Deacetylase InhibitorsAcetylationCyclin-Dependent Kinase Inhibitor p21DepsipeptidesDose-Response Relationship, DrugGene Expression RegulationHalf-LifeHumansLysinep300-CBP Transcription FactorsPhosphorylationPromoter Regions, GeneticProtein Processing, Post-TranslationalRNA, MessengerSerineSp1 Transcription FactorCyclin-Dependent Kinase Inhibitor p21DepsipeptidesHistone Deacetylase InhibitorsLysinep300-CBP Transcription FactorsRNA, MessengerromidepsinSerineSp1 Transcription FactorTumor Suppressor Protein p53

Identifiers

PMID16537920
PMCPMC1430330
OpenAlexW2161930186

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.