Evidence map›Paper›PMID 22569127›Full record

ArticleThe EMBO journal2012

The p57 CDKi integrates stress signals into cell-cycle progression to promote cell survival upon stress.

Manel Joaquin, Albert Gubern, Daniel González-Nuñez, E Josué Ruiz, Isabel Ferreiro, Eulalia de Nadal, Angel R Nebreda, Francesc Posas

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. CDK4/6 activity is required during GScience (New York, N.Y.) · 2024
    Article
  6. Review
  7. Cip1 tunes cell cycle arrest duration upon calcineurin activation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Article
  9. Regulation of p27Biomolecules · 2020
    Review
  10. Review
  11. The p38 Pathway: From Biology to Cancer Therapy.International journal of molecular sciences · 2020
    Review
  12. High Dosage Lithium Treatment Induces DNA Damage and p57International journal of molecular sciences · 2020
    Article
  13. Functional Versatility of the CDK Inhibitor p57Frontiers in cell and developmental biology · 2020
    Review
  14. Review
  15. Article
  16. Applied and environmental microbiology · 2019
    Article
  17. Article
  18. Knockdown ofOncology letters · 2018
    Article
  19. Article
  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

8 authors at 3 institutions in 1 country.

Manel JoaquinDepartament de Ciències Experimentals i de la Salut, Cell Signaling Research Group, Univeristat Pompeu Fabra, Barcelona, Spain. manel.joaquin@upf.edu
Albert Gubern
Daniel González-Nuñez
E Josué Ruiz
Isabel Ferreiro
Eulalia de Nadal
Angel R Nebreda
Francesc Posas
Pompeu Fabra University · ESInstitució Catalana de Recerca i Estudis Avançats · ESSpanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p57(Kip2) cyclin-dependent kinase inhibitor (CDKi) has been implicated in embryogenesis, stem-cell senescence and pathologies, but little is known of its role in cell cycle control. Here, we show that p57(Kip2) is targeted by the p38 stress-activated protein kinase (SAPK). Phosphorylation of p57(Kip2) at T143 by p38 enhances its association with and inhibition of Cdk2, which results in cell-cycle delay upon stress. Genetic inactivation of the SAPK or the CDKi abolishes cell-cycle delay upon osmostress and results in decreased cell viability. Oxidative stress and ionomycin also induce p38-mediated phosphorylation of p57 and cells lacking p38 or p57 display reduced viability to these stresses. Therefore, cell survival to various stresses depends on p57 phosphorylation by p38 that inhibits CDK activity. Together, these findings provide a novel molecular mechanism by which cells can delay cell cycle progression to maximize cell survival upon stress.

Indexed as

AnimalsCalcium IonophoresCell SurvivalCyclin-Dependent Kinase Inhibitor p57HEK293 CellsHumansIonomycinMiceOsmotic PressureOxidative Stressp38 Mitogen-Activated Protein KinasesPhosphorylationSignal TransductionCalcium IonophoresCDKN1C protein, humanCdkn1c protein, mouseCyclin-Dependent Kinase Inhibitor p57Ionomycinp38 Mitogen-Activated Protein Kinases

Identifiers

PMID22569127
PMCPMC3395087
OpenAlexW2160964662

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.