Evidence map›Paper›PMID 21301226›Full record

ArticleCell cycle (Georgetown, Tex.)2011

Nek1 kinase functions in DNA damage response and checkpoint control through a pathway independent of ATM and ATR.

Yumay Chen, Chi-Fen Chen, Daniel J Riley, Phang-Lang Chen

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

51 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  9. Article
  10. Targeting Prostate Cancer, the 'Tousled Way'.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Article
  13. In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Oligogenic Inheritance of MonoallelicFrontiers in genetics · 2021
    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

4 authors at 1 institution in 2 countries.

Yumay ChenDepartment of Medicine, University of California at Irvine, Irvine, CA USA. yumayc@uci.edu
Chi-Fen Chen
Daniel J Riley
Phang-Lang Chen
University of California, Irvine · US

Funding

Transgenic Animal and Morphology CoreP50DK061597 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HASTY, EDWARD PAUL · 2003 to 2007
$5.0M
Pathogenic Mechanism of Polycystic Kidney DiseaseR01DK067339 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CHEN, YUMAY · 2006 to 2010
$1.2M
Cell Cycle Dependent Mechanisms of Renal HypertrophyR01DK061626 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RILEY, DANIEL J · 2002 to 2006
$1.0M
NIDDK NIH HHS P50 DK061597NIDDK NIH HHS P50-DK61597NIDDK NIH HHS R01 DK061626NIDDK NIH HHS R01 DK067339NIDDK NIH HHS R01-DK067339NIDDK NIH HHS R01-DK61626
6 · The paper itself

Abstract

Never-in-mitosis A related protein kinase 1 (Nek1) is involved early in a DNA damage sensing/repair pathway. We have previously shown that cells without functional Nek1 fail to activate the more distal kinases Chk1 and Chk2 and fail to arrest properly at G1/S or M-phase checkpoints in response to DNA damage. As a consequence, foci of damaged DNA in Nek1 null cells persist long after the instigating insult, and Nek1 null cells develop unstable chromosomes at a rate much higher than identically cultured wild type cells. Here we show that Nek1 functions independently of canonical DNA damage responses requiring the PI3 kinase-like proteins ATM and ATR. Chemical inhibitors of ATM/ATR or mutation of the genes that encode them fail to alter the kinase activity of Nek1 or its localization to nuclear foci of DNA damage. Moreover ATM and ATR activities, including the localization of the proteins to DNA damage sites and phosphorylation of early DNA damage response substrates, are intact in Nek1 -/- murine cells and in human cells with Nek1 expression silenced by siRNA. Our results demonstrate that Nek1 is important for proper checkpoint control and characterize for the first time a DNA damage response that does not directly involve one of the known upstream mediator kinases, ATM or ATR.

Indexed as

DNA DamageDNA RepairAndrostadienesAnimalsAntibodiesAtaxia Telangiectasia Mutated ProteinsCarrier ProteinsCell Cycle ProteinsCheckpoint Kinase 1Checkpoint Kinase 2ChromonesDNA Breaks, Double-StrandedHumansMiceMorpholinesNIMA-Related Kinase 12-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAndrostadienesAntibodiesAtaxia Telangiectasia Mutated ProteinsATMIN protein, humanATR protein, humanCarrier ProteinsCell Cycle ProteinsCheckpoint Kinase 1Checkpoint Kinase 2CHEK1 protein, humanChek1 protein, mouseCHEK2 protein, humanChek2 protein, mouseChromonesMorpholinesNEK1 protein, humanNek1 protein, mouseNIMA-Related Kinase 1Nuclear ProteinsProtein KinasesProtein Serine-Threonine KinasesRNA, Small InterferingTranscription FactorsWortmannin

Identifiers

PMID21301226
PMCPMC3173995
OpenAlexW2046724857

What OpenQuestion 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 OpenQuestion graph.