Evidence map›Paper›PMID 24634213›Full record

ArticleThe Journal of biological chemistry2014

Src family kinases promote silencing of ATR-Chk1 signaling in termination of DNA damage checkpoint.

Yasunori Fukumoto, Mariko Morii, Takahito Miura, Sho Kubota, Kenichi Ishibashi, Takuya Honda, Aya Okamoto, Noritaka Yamaguchi, Atsushi Iwama, Yuji Nakayama and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024
    Review
  8. Review
  9. Article
  10. Attenuation of SRC Kinase Activity Augments PARP Inhibitor-mediated Synthetic Lethality inClinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  17. Review
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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

11 authors at 1 institution in 1 country.

Yasunori FukumotoFrom the Department of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba 260-8675, Japan and.
Mariko Morii
Takahito Miura
Sho Kubota
Kenichi Ishibashi
Takuya Honda
Aya Okamoto
Noritaka Yamaguchi
Atsushi Iwama
Yuji Nakayama
Naoto Yamaguchi
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA damage checkpoint arrests cell cycle progression to allow time for repair. Once DNA repair is completed, checkpoint signaling is terminated. Currently little is known about the mechanism by which checkpoint signaling is terminated, and the disappearance of DNA lesions is considered to induce the end of checkpoint signaling; however, here we show that the termination of checkpoint signaling is an active process promoted by Src family tyrosine kinases. Inhibition of Src activity delays recovery from the G2 phase DNA damage checkpoint following DNA repair. Src activity is required for the termination of checkpoint signaling, and inhibition of Src activity induces persistent activation of ataxia telangiectasia mutated (ATM)- and Rad3-related (ATR) and Chk1 kinases. Src-dependent nuclear protein tyrosine phosphorylation and v-Src expression suppress the ATR-mediated Chk1 and Rad17 phosphorylation induced by DNA double strand breaks or DNA replication stress. Thus, Src family kinases promote checkpoint recovery through termination of ATR- and Chk1-dependent G2 DNA damage checkpoint. These results suggest a model according to which Src family kinases send a termination signal between the completion of DNA repair and the initiation of checkpoint termination.

Indexed as

DNA DamageAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCheckpoint Kinase 1DNA RepairDown-RegulationDoxorubicinElectrophoresis, Polyacrylamide GelFlow CytometryG2 Phase Cell Cycle CheckpointsHeLa CellsHumansIndolesMicroscopy, FluorescenceNuclear ProteinsPhosphorylationAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanDoxorubicinIndolesNuclear ProteinsProtein KinasesRad17 protein, humansrc-Family KinasesSU 6656SulfonamidesTopoisomerase II InhibitorsTyrosineCell CycleCheckpoint ControlCheckpoint RecoveryDNA DamageDNA Damage ResponseSrc

Identifiers

PMID24634213
PMCPMC4007429
OpenAlexW2035206704

What Socratic holds

Textmetadata
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 Socratic graph.