Evidence map›Paper›PMID 19274768›Full record

ArticleEnvironmental and molecular mutagenesis2009

Mps1 as a link between centrosomes and genomic instability.

Christopher Kasbek, Ching-Hui Yang, Harold A Fisk

Open access · greenAbstract read
In one paragraph

Article in Environmental and molecular mutagenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. MPS1 inhibition as an anticancer strategy: where do we stand?Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026
    Review
  2. Mps1 is associated with the BRAFOncology letters · 2019
    Article
  3. Modular elements of the TPR domain in the Mps1 N terminus differentially target Mps1 to the centrosome and kinetochore.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
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  9. VDAC3 and Mps1 negatively regulate ciliogenesis.Cell cycle (Georgetown, Tex.) · 2013
    Article
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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

3 authors at 1 institution in 1 country.

Christopher KasbekDepartment of Molecular Genetics, The Ohio State University, 484 W. 12th Avenue, Columbus, OH 43210-1292, USA.
Ching-Hui Yang
Harold A Fisk
The Ohio State University · US

Funding

Regulation of the Mps1 Protein Kinase and Centrosome DuplicationR01GM077311 · NIGMS · OHIO STATE UNIVERSITY · PI FISK, HAROLD A · 2008 to 2012
$1.4M
NIGMS NIH HHS GM 77311NIGMS NIH HHS R01 GM077311
6 · The paper itself

Abstract

Centrosomes are microtubule-organizing centers that must be precisely duplicated before mitosis. Centrosomes regulate mitotic spindle assembly, and the presence of excess centrosomes leads to the production of aberrant mitotic spindles which generate chromosome segregation errors. Many human tumors possess excess centrosomes that lead to the production of abnormal spindles in situ. In some tumors, these extra centrosomes appear before aneuploidy, suggesting that defects in centrosome duplication might promote genomic instability and tumorigenesis. The Mps1 protein kinase is required for centrosome duplication, and preventing the proteasome-dependent degradation of Mps1 at centrosomes increases its local concentration and causes the production of excess centrosomes during a prolonged S-phase. Here, we show that Mps1 degradation is misregulated in two tumor-derived cell lines, and that the failure to appropriately degrade Mps1 correlates with the ability of these cells to produce extra centrosomes during a prolonged S-phase. In the 21NT breast-tumor derived cell line, a mutant Mps1 protein that is normally constitutively degraded can accumulate at centrosomes and perturb centrosome duplication, suggesting that these cells have a defect in the mechanisms that target Mps1 to the proteasome. In contrast, the U2OS osteosarcoma cell line expresses a nondegradable form of Mps1, which we show causes the dose-dependent over duplication of centrioles even at very low levels of expression. Our data demonstrate that defects in Mps1 degradation can occur through multiple mechanisms, and suggest that Mps1 may provide a link between the control of centrosome duplication and genomic instability.

Indexed as

CentrosomeGenomic InstabilityAllelesBlotting, WesternCell Cycle ProteinsCell Line, TumorHumansProtein Serine-Threonine KinasesProtein-Tyrosine KinasesReverse Transcriptase Polymerase Chain ReactionCell Cycle ProteinsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesTTK protein, human

Identifiers

PMID19274768
PMCPMC2760674
OpenAlexW1993331605

What OpenQuestion holds

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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.