Evidence map›Paper›PMID 27740454›Full record

ArticleeLife2016

Cyclin Kinase-independent role of p21

Sabrina F Mansilla, Agustina P Bertolin, Valérie Bergoglio, Marie-Jeanne Pillaire, Marina A González Besteiro, Carlos Luzzani, Santiago G Miriuka, Christophe Cazaux, Jean-Sébastien Hoffmann, Vanesa Gottifredi

Abstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Revisiting the Function of p21International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020
    Article
  18. Review
  19. Article
  20. Review
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.

Sabrina F MansillaFundación Instituto Leloir-Instituto de Investigaciones Bioquímicas de Buenos Aires, Consejo de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
Agustina P BertolinFundación Instituto Leloir-Instituto de Investigaciones Bioquímicas de Buenos Aires, Consejo de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
Valérie BergoglioCentre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Marie-Jeanne PillaireCentre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Marina A González BesteiroFundación Instituto Leloir-Instituto de Investigaciones Bioquímicas de Buenos Aires, Consejo de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
Carlos LuzzaniLaboratorio de Investigaciones Aplicadas en Neurociencias, Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia, Belén de Escobar, Argentina.
Santiago G MiriukaLaboratorio de Investigaciones Aplicadas en Neurociencias, Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia, Belén de Escobar, Argentina.ORCID 0000-0003-2402-3920
Christophe CazauxCentre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Jean-Sébastien HoffmannCentre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Vanesa GottifrediFundación Instituto Leloir-Instituto de Investigaciones Bioquímicas de Buenos Aires, Consejo de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.ORCID 0000-0001-9656-5951

Funding

THE ROLE OF P21 IN THE REPLICATION OF DAMAGED DNAR03TW008924 · FIC · FUNDACION INSTITUTO LELOIR · PI GOTTIFREDI, VANESA MONICA, PRIVES, CAROL · 2011 to 2013
$156k
FIC NIH HHS R03 TW008924
6 · The paper itself

Abstract

The levels of the cyclin-dependent kinase (CDK) inhibitor p21 are low in S phase and insufficient to inhibit CDKs. We show here that endogenous p21, instead of being residual, it is functional and necessary to preserve the genomic stability of unstressed cells. p21depletion slows down nascent DNA elongation, triggers permanent replication defects and promotes the instability of hard-to-replicate genomic regions, namely common fragile sites (CFS). The p21's PCNA interacting region (PIR), and not its CDK binding domain, is needed to prevent the replication defects and the genomic instability caused by p21 depletion. The alternative polymerase kappa is accountable for such defects as they were not observed after simultaneous depletion of both p21 and polymerase kappa. Hence, in CDK-independent manner, endogenous p21 prevents a type of genomic instability which is not triggered by endogenous DNA lesions but by a dysregulation in the DNA polymerase choice during genomic DNA synthesis.

Indexed as

Cell DivisionDNA ReplicationGenomic InstabilityCells, CulturedCyclin-Dependent Kinase Inhibitor p21DNAHumansCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNAcancer biologycell biologycommon fragile siteDNA elongationDNA replicationgenomic stabilityhumanp21 CDKN1A

Identifiers

PMID27740454
PMCPMC5120883

What OpenQuestion holds

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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.