Evidence map›Paper›PMID 29669289›Full record

ArticleCell reports2018

USP9X Limits Mitotic Checkpoint Complex Turnover to Strengthen the Spindle Assembly Checkpoint and Guard against Chromosomal Instability.

Agnieszka Skowyra, Lindsey A Allan, Adrian T Saurin, Paul R Clarke

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  10. Review
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  12. Mosaic Chromosomal Alterations Are Associated With Increased Lung Cancer Risk: Insight From the INTEGRAL-ILCCO Cohort Analysis.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

4 authors at 1 institution in 2 countries.

Agnieszka SkowyraDivision of Cancer Research, School of Medicine, University of Dundee, Jacqui Wood Cancer Centre, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK.
Lindsey A AllanDivision of Cancer Research, School of Medicine, University of Dundee, Jacqui Wood Cancer Centre, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK.
Adrian T SaurinDivision of Cancer Research, School of Medicine, University of Dundee, Jacqui Wood Cancer Centre, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK. Electronic address: a.saurin@dundee.ac.uk.
Paul R ClarkeDivision of Cancer Research, School of Medicine, University of Dundee, Jacqui Wood Cancer Centre, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK; The University of Queensland Diamantina Institute, Faculty of Medicine, Translational Research Institute, 37 Kent Street, Woolloongabba QLD 4102, Australia. Electronic address: paul.clarke@uq.edu.au.
Ninewells Hospital · GB

Funding

Cancer Research UK 13424Cancer Research UK 21229Cancer Research UK C275/A13424Cancer Research UK C47320/A21229Worldwide Cancer Research 12-0105
6 · The paper itself

Abstract

Faithful chromosome segregation during mitosis depends on the spindle assembly checkpoint (SAC), which delays progression through mitosis until every chromosome has stably attached to spindle microtubules via the kinetochore. We show here that the deubiquitinase USP9X strengthens the SAC by antagonizing the turnover of the mitotic checkpoint complex produced at unattached kinetochores. USP9X thereby opposes activation of anaphase-promoting complex/cyclosome (APC/C) and specifically inhibits the mitotic degradation of SAC-controlled APC/C substrates. We demonstrate that depletion or loss of USP9X reduces the effectiveness of the SAC, elevates chromosome segregation defects, and enhances chromosomal instability (CIN). These findings provide a rationale to explain why loss of USP9X could be either pro- or anti-tumorigenic depending on the existing level of CIN.

Indexed as

MitosisAnaphase-Promoting Complex-CyclosomeApc11 Subunit, Anaphase-Promoting Complex-CyclosomeCdc20 ProteinsChromosomal InstabilityChromosome SegregationCyclin BHeLa CellsHumansKaryotypeKinesinsKinetochoresNIMA-Related KinasesNocodazoleRNA InterferenceRNA, Small InterferingANAPC11 protein, humanAnaphase-Promoting Complex-CyclosomeApc11 Subunit, Anaphase-Promoting Complex-CyclosomeCDC20 protein, humanCdc20 ProteinsCyclin BKIF18A protein, humanKinesinsNEK2 protein, humanNIMA-Related KinasesNocodazoleRNA, Small InterferingUbiquitin ThiolesteraseUSP9X protein, humanAPC/CcancerCdc20chromosomal instabilitycyclindeubiquitinaseMcl-1mitosisspindle assembly checkpointUSP9X

Identifiers

PMID29669289
PMCPMC5917450
OpenAlexW2802052189

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.