Evidence map›Paper›PMID 26743940›Full record

ArticleNature communications2016

Cep57 is a Mis12-interacting kinetochore protein involved in kinetochore targeting of Mad1-Mad2.

Haining Zhou, Tianning Wang, Tao Zheng, Junlin Teng, Jianguo Chen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
  5. Article
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  7. Review
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  9. Article
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  11. Article
  12. MAD1: Kinetochore Receptors and Catalytic Mechanisms.Frontiers in cell and developmental biology · 2018
    Review
  13. Article
  14. Article
  15. 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

5 authors at 3 institutions in 1 country.

Haining ZhouKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education and State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing 100871, China.
Tianning WangKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education and State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing 100871, China.
Tao ZhengKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education and State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing 100871, China.
Junlin TengKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education and State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing 100871, China.
Jianguo ChenKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education and State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing 100871, China.
Peking University · CNState Key Laboratory of Membrane BiologyCenter for Life Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The spindle assembly checkpoint (SAC) arrests cells in mitosis by sensing unattached kinetochores, until all chromosomes are bi-oriented by spindle microtubules. Kinetochore accumulation of the SAC component Mad1-Mad2 is crucial for SAC activation. However, the mechanism by which Mad1-Mad2 accumulation at kinetochores is regulated is not clear. Here we find that Cep57 is localized to kinetochores in human cells, and binds to Mis12, a KMN (KNL1/Mis12 complex/Ndc80 complex) network component. Cep57 also interacts with Mad1, and depletion of Cep57 results in decreased kinetochore localization of Mad1-Mad2, reduced SAC signalling and increased chromosome segregation errors. We also show that the microtubule-binding activity of Cep57 is involved in the timely removal of Mad1 from kinetochores. Thus, these findings reveal that the KMN network-binding protein Cep57 is a mitotic kinetochore component, and demonstrate the functional connection between the KMN network and the SAC.

Indexed as

M Phase Cell Cycle CheckpointsCell Cycle ProteinsCell LineChromosome SegregationCytoskeletal ProteinsHEK293 CellsHeLa CellsHumansKinetochoresMad2 ProteinsMicroscopy, FluorescenceMicrotubule-Associated ProteinsMicrotubulesNuclear ProteinsOrganisms, Genetically ModifiedPolymerizationCell Cycle ProteinsCEP57 protein, humanCytoskeletal ProteinsKnl1 protein, humanMAD1L1 protein, humanMAD2L1 protein, humanMad2 ProteinsMicrotubule-Associated ProteinsMIS12 protein, humanNDC80 protein, humanNuclear Proteins

Identifiers

PMID26743940
PMCPMC4729865
OpenAlexW2254585873

What OpenQuestion holds

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Registered trials

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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.