Evidence map›Paper›PMID 24219989›Full record

ArticleThe EMBO journal2013

Acetylation of p53 stimulates miRNA processing and determines cell survival following genotoxic stress.

Jonathan Chang, Brandi N Davis-Dusenbery, Risa Kashima, Xuan Jiang, Nisha Marathe, Roberto Sessa, Justin Louie, Wei Gu, Giorgio Lagna, Akiko Hata

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Regulation of miRNAs Expression by Mutant p53 Gain of Function in Cancer.Frontiers in cell and developmental biology · 2021
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Complexity in regulating microRNA biogenesis in cancer.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  12. Article
  13. Article
  14. Post-Transcriptional Regulation of Anti-Apoptotic BCL2 Family Members.International journal of molecular sciences · 2018
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

10 authors at 4 institutions in 1 country.

Jonathan Chang1] Cardiovascular Research Institute, University of California, San Francisco, CA, USA [2] Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA, USA [3] Department of Biochemistry, Tufts University School of Medicine, Boston, MA, USA.
Brandi N Davis-Dusenbery
Risa Kashima
Xuan Jiang
Nisha Marathe
Roberto Sessa
Justin Louie
Wei Gu
Giorgio Lagna
University of California, San Francisco · USCancer Genetics (United States) · USTufts Medical Center · USTufts 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
Regulation of p53 acetylation and deacetylation in tumorigenesis.R01CA085533 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2000 to 2021
$5.2M
Role of miRNAs in Vascular PhysiologyR01HL093154 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HATA, AKIKO · 2009 to 2012
$1.6M
Role of the PDGF signaling pathway in pulmonary artery hypertensionR01HL116191 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HATA, AKIKO · 2013 to 2016
$1.5M
Mechanisms of TGFB Signal TransductionR01HL108317 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HATA, AKIKO · 2011 to 2014
$1.5M
NCI NIH HHS CA080058NCI NIH HHS CA85533NCI NIH HHS P01 CA080058NCI NIH HHS R01 CA085533NHLBI NIH HHS HL093154NHLBI NIH HHS HL108317NHLBI NIH HHS R01 HL093154NHLBI NIH HHS R01 HL108317NHLBI NIH HHS R01 HL116191
6 · The paper itself

Abstract

It is widely accepted that different forms of stress activate a common target, p53, yet different outcomes are triggered in a stress-specific manner. For example, activation of p53 by genotoxic agents, such as camptothecin (CPT), triggers apoptosis, while non-genotoxic activation of p53 by Nutlin-3 (Nut3) leads to cell-cycle arrest without significant apoptosis. Such stimulus-specific responses are attributed to differential transcriptional activation of various promoters by p53. In this study, we demonstrate that CPT, but not Nut3, induces miR-203, which downregulates anti-apoptotic bcl-w and promotes cell death in a p53-dependent manner. We find that acetylation of K120 in the DNA-binding domain of p53 augments its association with the Drosha microprocessor and promotes nuclear primary miRNA processing. Knockdown of human orthologue of Males absent On the First (hMOF), the acetyltransferase that targets K120 in p53, abolishes induction of miR-203 and cell death mediated by CPT. Thus, this study reveals that p53 acetylation at K120 plays a critical role in the regulation of the Drosha microprocessor and that post-transcriptional regulation of gene expression by p53 via miRNAs plays a role in determining stress-specific cellular outcomes.

Indexed as

DNA DamageAcetylationApoptosis Regulatory ProteinsCamptothecinCell SurvivalHCT116 CellsHistone AcetyltransferasesHumansImidazolesMicroRNAsPiperazinesPromoter Regions, GeneticRibonuclease IIIRNA Processing, Post-TranscriptionalTumor Suppressor Protein p53Apoptosis Regulatory ProteinsBCL2L2 protein, humanCamptothecinDROSHA protein, humanHistone AcetyltransferasesImidazolesKAT8 protein, humanMicroRNAsMIRN203 microRNA, humannutlin 3PiperazinesRibonuclease IIITumor Suppressor Protein p53

Identifiers

PMID24219989
PMCPMC3981142
OpenAlexW2096268559

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.