Evidence map›Paper›PMID 27611996›Full record

ArticlePloS one2016

p27Kip1 Is Required to Mediate a G1 Cell Cycle Arrest Downstream of ATM following Genotoxic Stress.

Erica K Cassimere, Claire Mauvais, Catherine Denicourt

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Loss of fragile WWOX gene leads to senescence escape and genome instability.Cellular and molecular life sciences : CMLS · 2023
    Article
  6. Article
  7. p27, The Cell Cycle and Alzheimer´s Disease.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Regulation of p27Biomolecules · 2020
    Review
  10. Contributions of DNA Damage to Alzheimer's Disease.International journal of molecular sciences · 2020
    Review
  11. High Dosage Lithium Treatment Induces DNA Damage and p57International journal of molecular sciences · 2020
    Article
  12. WIP1 dephosphorylation of p27Cell cycle (Georgetown, Tex.) · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Loss of p27Scientific reports · 2017
    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

3 authors at 1 institution in 1 country.

Erica K CassimereDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center, Houston, Texas, United States of America.
Claire MauvaisDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center, Houston, Texas, United States of America.
Catherine DenicourtDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center, Houston, Texas, United States of America.
The University of Texas Health Science Center at Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA damage response (DDR) is a coordinated signaling network that ensures the maintenance of genome stability under DNA damaging stress. In response to DNA lesions, activation of the DDR leads to the establishment of cell cycle checkpoints that delay cell-cycle progression and allow repair of the defects. The tumor suppressor p27Kip1 is a cyclin-CDK inhibitor that plays an important role in regulating quiescence in a variety of tissues. Several studies have suggested that p27Kip1 also plays a role in the maintenance of genomic integrity. Here we demonstrate that p27Kip1 is essential for the establishment of a G1 checkpoint arrest after DNA damage. We also uncovered that ATM phosphorylates p27Kip1 on a previously uncharacterized residue (Ser-140), which leads to its stabilization after induction of DNA double-strand breaks. Inhibition of this stabilization by replacing endogenous p27Kip1 with a Ser-140 phospho-mutant (S140A) significantly sensitized cells to IR treatments. Our findings reveal a novel role for p27Kip1 in the DNA damage response pathway and suggest that part of its tumor suppressing functions relies in its ability to mediate a G1 arrest after the induction of DNA double strand breaks.

Indexed as

DNA DamageG1 Phase Cell Cycle CheckpointsSignal TransductionAtaxia Telangiectasia Mutated ProteinsCell LineCell SurvivalCyclin-Dependent Kinase Inhibitor p27DNA Breaks, Double-StrandedG1 PhaseGamma RaysHumansPhosphorylationPhosphoserineProtein StabilityS PhaseSpheroids, CellularAtaxia Telangiectasia Mutated ProteinsCyclin-Dependent Kinase Inhibitor p27Phosphoserine

Identifiers

PMID27611996
PMCPMC5017644
OpenAlexW2507519213

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.