Evidence map›Paper›PMID 26953350›Full record

ArticleThe Journal of cell biology2016

ARHGEF17 is an essential spindle assembly checkpoint factor that targets Mps1 to kinetochores.

Mayumi Isokane, Thomas Walter, Robert Mahen, Bianca Nijmeijer, Jean-Karim Hériché, Kota Miura, Stefano Maffini, Miroslav Penchev Ivanov, Tomoya S Kitajima, Jan-Michael Peters and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 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
1.7field-weighted citation impact, top 18% 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, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Case report: Expanding the phenotype ofFrontiers in neurology · 2022
    Article
  4. Article
  5. Article
  6. Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Mayumi IsokaneCell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Thomas WalterCell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Robert MahenCell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Bianca NijmeijerCell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Jean-Karim HérichéCell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Kota MiuraCentre for Molecular and Cellular Imaging, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Stefano MaffiniDepartment of Mechanistic Cell Biology, Max Planck Institute of Molecular Physiology, 44227 Dortmund, Germany.
Miroslav Penchev IvanovMolecular and Cellular Biology, Research Institute of Molecular Pathology, 1030 Vienna, Austria.
Tomoya S KitajimaCell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Jan-Michael PetersMolecular and Cellular Biology, Research Institute of Molecular Pathology, 1030 Vienna, Austria.
Jan EllenbergCell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany jan.ellenberg@embl.de.
European Molecular Biology Laboratory · DEResearch Institute of Molecular Pathology · ATEuropean Molecular Biology Laboratory · DEMax Planck Institute of Molecular Physiology · DE

Funding

Wellcome TrustWellcome Trust 100090/Z/12/Z
6 · The paper itself

Abstract

To prevent genome instability, mitotic exit is delayed until all chromosomes are properly attached to the mitotic spindle by the spindle assembly checkpoint (SAC). In this study, we characterized the function of ARHGEF17, identified in a genome-wide RNA interference screen for human mitosis genes. Through a series of quantitative imaging, biochemical, and biophysical experiments, we showed that ARHGEF17 is essential for SAC activity, because it is the major targeting factor that controls localization of the checkpoint kinase Mps1 to the kinetochore. This mitotic function is mediated by direct interaction of the central domain of ARHGEF17 with Mps1, which is autoregulated by the activity of Mps1 kinase, for which ARHGEF17 is a substrate. This mitosis-specific role is independent of ARHGEF17's RhoGEF activity in interphase. Our study thus assigns a new mitotic function to ARHGEF17 and reveals the molecular mechanism for a key step in SAC establishment.

Indexed as

Cell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorHeLa CellsHumansKinetochoresMitosisProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRho Guanine Nucleotide Exchange FactorsSignal TransductionSpindle ApparatusARHGEF17 protein, humanCell Cycle ProteinsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRho Guanine Nucleotide Exchange FactorsTTK protein, human

Identifiers

PMID26953350
PMCPMC4792069
OpenAlexW2293021919

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.