Evidence map›Paper›PMID 20463968›Full record

ArticlePloS one2010

p53-induced growth arrest is regulated by the mitochondrial SirT3 deacetylase.

SiDe Li, Michaela Banck, Shiraz Mujtaba, Ming-Ming Zhou, Mary M Sugrue, Martin J Walsh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

87 citing papers in PubMed, 151 citations in OpenAlex.

  1. Trial
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  7. EBNA1 Upregulates P53-Inhibiting Genes in Burkitt's Lymphoma Cell Line.Reports of biochemistry & molecular biology · 2023
    Article
  8. Article
  9. Review
  10. Role of sirtuins in esophageal cancer: Current status and future prospects.World journal of gastrointestinal oncology · 2022
    Review
  11. Mitochondrial sirtuin 3 and various cell death modalities.Frontiers in cell and developmental biology · 2022
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
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  20. Article

27 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

6 authors at 2 institutions in 1 country.

SiDe LiDepartment of Pediatrics, Mount Sinai School of Medicine, New York, New York, United States of America.
Michaela Banck
Shiraz Mujtaba
Ming-Ming Zhou
Mary M Sugrue
Martin J Walsh
Icahn School of Medicine at Mount Sinai · USWinnMed · US

Funding

Chemical Genomics Paradigm for Epigentic RegulationR01HG004508 · NHGRI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ZHOU, MING-MING · 2008 to 2014
$6.7M
Regulation of Irreversible Growth Arrest by p53R01CA098552 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI SUGRUE, MARY M · 2003 to 2007
$1.2M
Regulation of CFTR gene expressionR01HL067099 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI WALSH, MARTIN JOHN · 2001 to 2004
$1.2M
A Novel Epigenetic Gene Silencing TechnologyRC1DA028776 · NIDA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI WALSH, MARTIN JOHN, ZHOU, MING-MING · 2009 to 2010
$977k
NCI NIH HHS CA98552NCI NIH HHS R01 CA098552NHGRI NIH HHS R01 HG004508NHLBI NIH HHS HL67099NHLBI NIH HHS R01 HL067099NIDA NIH HHS RC1 DA028776
6 · The paper itself

Abstract

A hallmark of p53 function is to regulate a transcriptional program in response to extracellular and intracellular stress that directs cell cycle arrest, apoptosis, and cellular senescence. Independent of the role of p53 in the nucleus, some of the anti-proliferative functions of p53 reside within the mitochondria [1]. p53 can arrest cell growth in response to mitochondrial p53 in an EJ bladder carcinoma cell environment that is naïve of p53 function until induced to express p53 [2]. TP53 can independently partition with endogenous nuclear and mitochondrial proteins consistent with the ability of p53 to enact senescence. In order to address the role of p53 in navigating cellular senescence through the mitochondria, we identified SirT3 to rescue EJ/p53 cells from induced p53-mediated growth arrest. Human SirT3 function appears coupled with p53 early during the initiation of p53 expression in the mitochondria by biochemical and cellular localization analysis. Our evidence suggests that SirT3 partially abrogates p53 activity to enact growth arrest and senescence. Additionally, we identified the chaperone protein BAG-2 in averting SirT3 targeting of p53 -mediated senescence. These studies identify a complex relationship between p53, SirT3, and chaperoning factor BAG-2 that may link the salvaging and quality assurance of the p53 protein for control of cellular fate independent of transcriptional activity.

Indexed as

AcetylationCell Line, TumorCell ProliferationCellular SenescenceGene DeletionHSP70 Heat-Shock ProteinsHumansMitochondriaMolecular ChaperonesNADPhenotypeProtein BindingProtein StabilityProtein Structure, TertiaryProtein TransportProto-Oncogene Proteins c-bcl-2BAG2 protein, humanHSP70 Heat-Shock ProteinsMolecular ChaperonesNADProto-Oncogene Proteins c-bcl-2SIRT3 protein, humanSirtuin 3Tumor Suppressor Protein p53

Identifiers

PMID20463968
PMCPMC2864751
OpenAlexW2078229478

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.