Evidence map›Paper›PMID 28017606›Full record

ArticleCurrent biology : CB2017

Generation of a Spindle Checkpoint Arrest from Synthetic Signaling Assemblies.

Ivan Yuan, Ioanna Leontiou, Priya Amin, Karen M May, Sadhbh Soper Ní Chafraidh, Eliška Zlámalová, Kevin G Hardwick

Open access · hybridAbstract read
In one paragraph

Article in Current biology : CB, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  7. Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021
    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

7 authors at 2 institutions in 1 country.

Ivan YuanWellcome Trust Centre for Cell Biology, University of Edinburgh King's Buildings, Max Born Crescent, Edinburgh EH9 3BF, UK.
Ioanna LeontiouWellcome Trust Centre for Cell Biology, University of Edinburgh King's Buildings, Max Born Crescent, Edinburgh EH9 3BF, UK.
Priya AminWellcome Trust Centre for Cell Biology, University of Edinburgh King's Buildings, Max Born Crescent, Edinburgh EH9 3BF, UK.
Karen M MayWellcome Trust Centre for Cell Biology, University of Edinburgh King's Buildings, Max Born Crescent, Edinburgh EH9 3BF, UK.
Sadhbh Soper Ní ChafraidhWellcome Trust Centre for Cell Biology, University of Edinburgh King's Buildings, Max Born Crescent, Edinburgh EH9 3BF, UK.
Eliška ZlámalováWellcome Trust Centre for Cell Biology, University of Edinburgh King's Buildings, Max Born Crescent, Edinburgh EH9 3BF, UK.
Kevin G HardwickWellcome Trust Centre for Cell Biology, University of Edinburgh King's Buildings, Max Born Crescent, Edinburgh EH9 3BF, UK. Electronic address: kevin.hardwick@ed.ac.uk.
Wellcome Centre for Cell Biology · GBUniversity of Edinburgh · GB

Funding

Wellcome Trust 092076
6 · The paper itself

Abstract

The spindle checkpoint acts as a mitotic surveillance system, monitoring interactions between kinetochores and spindle microtubules and ensuring high-fidelity chromosome segregation [1-3]. The checkpoint is activated by unattached kinetochores, and Mps1 kinase phosphorylates KNL1 on conserved MELT motifs to generate a binding site for the Bub3-Bub1 complex [4-7]. This leads to dynamic kinetochore recruitment of Mad proteins [8, 9], a conformational change in Mad2 [10-12], and formation of the mitotic checkpoint complex (MCC: Cdc20-Mad3-Mad2 [13-15]). MCC formation inhibits the anaphase-promoting complex/cyclosome (Cdc20-APC/C), thereby preventing the proteolytic destruction of securin and cyclin and delaying anaphase onset. What happens at kinetochores after Mps1-dependent Bub3-Bub1 recruitment remains mechanistically unclear, and it is not known whether kinetochore proteins other than KNL1 have significant roles to play in checkpoint signaling and MCC generation. Here, we take a reductionist approach, avoiding the complexities of kinetochores, and demonstrate that co-recruitment of KNL1

Indexed as

Cell Cycle CheckpointsChromosome SegregationMitosisSignal TransductionKinetochoresMicrotubulesPhosphorylationSchizosaccharomycesSchizosaccharomyces pombe ProteinsSpindle ApparatusSchizosaccharomyces pombe ProteinsBubcell cyclecheckpointkinetochoreMadmitosisMps1spindlesynthetic

Identifiers

PMID28017606
PMCPMC5226922
OpenAlexW2559300329

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.