Evidence map›Paper›PMID 19079133›Full record

ArticleEMBO reports2009

Cellular senescence and organismal ageing in the absence of p21(CIP1/WAF1) in ku80(-/-) mice.

Bo Zhao, Erica K Benson, Ruifang Qiao, Xing Wang, Sunchin Kim, James J Manfredi, Sam W Lee, Stuart A Aaronson

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in EMBO reports, 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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Constitutive, Muscle-SpecificBiomedicines · 2024
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. REGγ deficiency promotes premature aging via the casein kinase 1 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Bo ZhaoDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.
Erica K Benson
Ruifang Qiao
Xing Wang
Sunchin Kim
James J Manfredi
Sam W Lee
Stuart A Aaronson
Icahn School of Medicine at Mount Sinai · USMassachusetts General Hospital · 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
CELLULAR SENESCENCE IN AGING AND CANCERR01CA085214 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI AARONSON, STUART A · 1999 to 2008
$3.9M
Cyclin G in p53 mediated pathways and breast cancerR01CA085681 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LEE, SAM W · 2001 to 2011
$2.6M
Role of an unusual GTPase in DNA damage response and carcinogenesisR01CA127247 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LEE, SAM W · 2008 to 2012
$1.7M
NCI NIH HHS 1R01CA127247NCI NIH HHS 2R01CA085681NCI NIH HHS 5P01CA080058NCI NIH HHS 5R01CA085214NCI NIH HHS P01 CA080058NCI NIH HHS R01 CA085214NCI NIH HHS R01 CA085681NCI NIH HHS R01 CA127247
6 · The paper itself

Abstract

Ku80 is important in the repair of DNA double-strand breaks by its essential function in non-homologous end-joining. The absence of Ku80 causes the accumulation of DNA damage and leads to premature ageing in mice. We showed that mouse embryonic fibroblasts (MEFs) from ku80(-/-) mice senesced rapidly with elevated levels of p53 and p21. Deletion of p21 delayed the early senescence phenotype in ku80(-/-) MEFs, despite an otherwise intact response of p53. In contrast to ku80(-/-)p53(-/-) mice, which die rapidly primarily from lymphomas, there was no significant increase in tumorigenesis in ku80(-/-)p21(-/-) mice. However, ku80(-/-)p21(-/-) mice showed no improvement with respect to rough fur coat or osteopaenia, and even showed a shortened lifespan compared with ku80(-/-) mice. These results show that the increased lifespan of ku80(-/-) MEFs owing to the loss of p21 is not associated with an improvement of the premature ageing phenotypes of ku80(-/-) mice observed at the organismal level.

Indexed as

AgingAnimalsAntigens, NuclearCell LineCell Transformation, NeoplasticCellular SenescenceCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsFibroblastsG1 PhaseGene DeletionKu AutoantigenMiceMice, KnockoutPhenotypeSurvival RateAntigens, NuclearCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsKu AutoantigenTumor Suppressor Protein p53Xrcc6 protein, mouse

Identifiers

PMID19079133
PMCPMC2613205
OpenAlexW2054079671

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.