Evidence map›Paper›PMID 19289837›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

The DNA-damage effector checkpoint kinase 1 is essential for chromosome segregation and cytokinesis.

Sirisha Peddibhotla, Michael H Lam, Maria Gonzalez-Rimbau, Jeffrey M Rosen

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 105 citations in OpenAlex.

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  9. On the assembly of the mitotic spindle, bistability and hysteresis.Cellular and molecular life sciences : CMLS · 2023
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  19. Checkpoint kinase 1-induced phosphorylation ofThe Journal of biological chemistry · 2017
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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

4 authors at 2 institutions in 2 countries.

Sirisha PeddibhotlaInterdepartmental Program in Cell and Molecular Biology and Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Michael H Lam
Maria Gonzalez-Rimbau
Jeffrey M Rosen
Baylor College of Medicine · USInstitute of Molecular and Cell Biology · RU

Funding

MALAT1 lncRNA as a Therapeutic Target in Triple Negative Breast CancerR01CA016303 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ROSEN, JEFFREY MARK · 1985 to 2022
$8.1M
HORMONAL REGULATION OF BREAST CANCERR37CA016303 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ROSEN, JEFFREY MARK · 1989 to 2011
$7.3M
NCI NIH HHS CA 16303NCI NIH HHS R01 CA016303NCI NIH HHS R37 CA016303
6 · The paper itself

Abstract

Defective genome maintenance mechanisms, involving DNA repair and cell-cycle checkpoint pathways, initiate genetic instability in many sporadic and hereditary cancers. The DNA damage effector Checkpoint kinase 1 (Chk1) is a critical component of DNA replication, intra-S phase, and G(2)/M phase checkpoints and a recently reported mitotic spindle-assembly checkpoint. Here, we report for the first time that haploinsufficiency of Chk1 in mice resulted in multiple mitotic defects and enhanced binucleation. We observed that Aurora B, a critical cytokinetic regulator and a recently identified Chk1 substrate, was mislocalized in mitotic Chk1(+/-) mammary epithelia. Chk1 also exhibited distinct mitotic localization patterns and was active during unperturbed mitosis and cytokinesis in mammalian cells. Active Chk1 expression was not dependent on treatment with spindle poisons such as colcemid during mitosis and cytokinesis. Furthermore, two different complementary approaches demonstrated that abrogation of Chk1 in mitotic mammalian cells resulted in cytokinetic regression and binucleation, increased chromosome lagging and/or nondisjunction, and abnormal localization of Aurora B at late mitotic structures. Thus, Chk1 is a multifunctional kinase that serves as a nexus between the DNA damage response and the mitotic exit pathways during cell-cycle progression to prevent genomic instability and cancer.

Indexed as

Chromosome SegregationCytokinesisDNA DamageAnimalsAurora Kinase BAurora KinasesCheckpoint Kinase 1Epithelial CellsHaplotypesMiceMitosisProtein KinasesProtein Serine-Threonine KinasesAurkb protein, mouseAurora Kinase BAurora KinasesCheckpoint Kinase 1Chek1 protein, mouseProtein KinasesProtein Serine-Threonine Kinases

Identifiers

PMID19289837
PMCPMC2663996
OpenAlexW2003884609

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.