Evidence map›Paper›PMID 30341343›Full record

ArticleNature communications2018

TRIP13 and APC15 drive mitotic exit by turnover of interphase- and unattached kinetochore-produced MCC.

Dong Hyun Kim, Joo Seok Han, Peter Ly, Qiaozhen Ye, Moira A McMahon, Kyungjae Myung, Kevin D Corbett, Don W Cleveland

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 56 citations in OpenAlex.

  1. Dual Inhibition of TRIP13 and Aurora A Induces Mitotic DNA Damage and Concurrent Pyroptotic-Apoptotic Cell Death in Rb-Deficient Cancer Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  2. Article
  3. Article
  4. Science advances · 2025
    Article
  5. Article
  6. CCDC68 Maintains Mitotic Checkpoint Activation by Promoting CDC20 Integration into the MCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  7. Article
  8. The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024
    Review
  9. Article
  10. Principles and dynamics of spindle assembly checkpoint signalling.Nature reviews. Molecular cell biology · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021
    Review
  19. Article
  20. p31Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

8 authors at 4 institutions in 3 countries.

Dong Hyun KimLudwig Institute for Cancer Research, San Diego Branch, La Jolla, CA, 92093, USA.
Joo Seok HanCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan, 44919, Republic of Korea.
Peter LyLudwig Institute for Cancer Research, San Diego Branch, La Jolla, CA, 92093, USA.ORCID http://orcid.org/0000-0001-8946-7069
Qiaozhen YeDepartment of Cellular and Molecular Medicine, University of California-San Diego, La Jolla, CA, 92093, USA.
Moira A McMahonLudwig Institute for Cancer Research, San Diego Branch, La Jolla, CA, 92093, USA.
Kyungjae MyungCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan, 44919, Republic of Korea.
Kevin D CorbettDepartment of Cellular and Molecular Medicine, University of California-San Diego, La Jolla, CA, 92093, USA. kcorbett@ucsd.edu.ORCID http://orcid.org/0000-0001-5854-2388
Don W ClevelandLudwig Institute for Cancer Research, San Diego Branch, La Jolla, CA, 92093, USA. dcleveland@ucsd.edu.
University of California San Diego · USInstitute for Basic Science · KRIonis Pharmaceuticals (United States) · USLudwig Cancer Research · BE

Funding

Mechanisms of chromosome segregation, aneuploidy, and tumorigenesisR35GM122476 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Don W Cleveland · 2017 to 2026
$9.0M
MICROTUBULE REGULATIONR01GM029513 · NIGMS · LUDWIG INSTITUTE FOR CANCER RES LTD · PI CLEVELAND, DON W · 1985 to 2016
$8.2M
Molecular mechanisms of chromosome organization and recombination control by the meiotic chromosome axis.R01GM104141 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CORBETT, KEVIN DANIEL · 2013 to 2021
$3.1M
Cell Division Errors as a Mechanism Driving Massive Genomic RearrangementsK99CA218871 · NCI · LUDWIG INSTITUTE FOR CANCER RES LTD · PI LY, PETER · 2017 to 2018
$236k
NCI NIH HHS K99 CA218871NIGMS NIH HHS R01 GM029513NIGMS NIH HHS R01 GM104141NIGMS NIH HHS R35 GM122476U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) K99 CA218871U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R01 GM104141U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R01 GM2951U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35 GM122476
6 · The paper itself

Abstract

The mitotic checkpoint ensures accurate chromosome segregation through assembly of the mitotic checkpoint complex (MCC), a soluble inhibitor of the anaphase-promoting complex/cyclosome (APC/C) produced by unattached kinetochores. MCC is also assembled during interphase by Mad1/Mad2 bound at nuclear pores, thereby preventing premature mitotic exit prior to kinetochore maturation and checkpoint activation. Using degron tagging to rapidly deplete the AAA+ ATPase TRIP13, we show that its catalytic activity is required to maintain a pool of open-state Mad2 for MCC assembly, thereby supporting mitotic checkpoint activation, but is also required for timely mitotic exit through catalytic disassembly of MCC. Strikingly, combining TRIP13 depletion with elimination of APC15-dependent Cdc20 ubiquitination/degradation results in a complete inability to exit mitosis, even when MCC assembly at unattached kinetochores is prevented. Thus, mitotic exit requires MCC produced either in interphase or mitosis to be disassembled by TRIP13-catalyzed removal of Mad2 or APC15-driven ubiquitination/degradation of its Cdc20 subunit.

Indexed as

M Phase Cell Cycle CheckpointsAnaphase-Promoting Complex-CyclosomeATPases Associated with Diverse Cellular ActivitiesCdc20 ProteinsCell Cycle ProteinsInterphaseKinetochoresMad2 ProteinsMitosisANAPC15 protein, humanAnaphase-Promoting Complex-CyclosomeATPases Associated with Diverse Cellular ActivitiesCDC20 protein, humanCdc20 ProteinsCell Cycle ProteinsMAD2L1 protein, humanMad2 ProteinsTRIP13 protein, human

Identifiers

PMID30341343
PMCPMC6195577
OpenAlexW2896661771

What OpenQuestion holds

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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.