Evidence map›Paper›PMID 26527744›Full record

ArticleThe Journal of cell biology2015

TRIP13PCH-2 promotes Mad2 localization to unattached kinetochores in the spindle checkpoint response.

Christian R Nelson, Tom Hwang, Pin-Hsi Chen, Needhi Bhalla

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of TRIP13 in human cancer development.Molecular biology reports · 2024
    Review
  4. Principles and dynamics of spindle assembly checkpoint signalling.Nature reviews. Molecular cell biology · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. p31Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. The conserved AAA-ATPase PCH-2Molecular biology of the cell · 2020
    Article
  11. Disassembly of the Shieldin Complex by TRIP13.Cell cycle (Georgetown, Tex.) · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Christian R NelsonDepartment of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, Santa Cruz, CA 95064.
Tom HwangDepartment of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, Santa Cruz, CA 95064.
Pin-Hsi ChenDepartment of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, Santa Cruz, CA 95064.
Needhi BhallaDepartment of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, Santa Cruz, CA 95064 nbhalla@ucsc.edu.
University of California, Santa Cruz · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Training Program/Molecular/Cell/Developmental BiologyT32GM008646 · NIGMS · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI STROME, SUSAN · 1999 to 2018
$3.7M
The Synapsis Checkpoint in C. elegans MeiosisR01GM097144 · NIGMS · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI BHALLA, NEEDHI · 2011 to 2020
$2.8M
NIGMS NIH HHS R01 GM097144NIGMS NIH HHS R01GM097144NIGMS NIH HHS T32 GM008646NIGMS NIH HHS T32GM008646NIH HHS P40 OD010440
6 · The paper itself

Abstract

The spindle checkpoint acts during cell division to prevent aneuploidy, a hallmark of cancer. During checkpoint activation, Mad1 recruits Mad2 to kinetochores to generate a signal that delays anaphase onset. Yet, whether additional factors contribute to Mad2's kinetochore localization remains unclear. Here, we report that the conserved AAA+ ATPase TRIP13(PCH-2) localizes to unattached kinetochores and is required for spindle checkpoint activation in Caenorhabditis elegans. pch-2 mutants effectively localized Mad1 to unattached kinetochores, but Mad2 recruitment was significantly reduced. Furthermore, we show that the C. elegans orthologue of the Mad2 inhibitor p31(comet)(CMT-1) interacts with TRIP13(PCH-2) and is required for its localization to unattached kinetochores. These factors also genetically interact, as loss of p31(comet)(CMT-1) partially suppressed the requirement for TRIP13(PCH-2) in Mad2 localization and spindle checkpoint signaling. These data support a model in which the ability of TRIP13(PCH-2) to disassemble a p31(comet)/Mad2 complex, which has been well characterized in the context of checkpoint silencing, is also critical for spindle checkpoint activation.

Indexed as

Adaptor Proteins, Signal TransducingAdenosine TriphosphatasesAnimal HusbandryAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCarrier ProteinsCell Cycle CheckpointsCell Cycle ProteinsKinetochoresMad2 ProteinsNuclear ProteinsSignal TransductionSpindle ApparatusAdaptor Proteins, Signal TransducingAdenosine TriphosphatasesCaenorhabditis elegans ProteinsCarrier ProteinsCell Cycle ProteinsMad2 ProteinsMDF-1 protein, C elegansNuclear ProteinsPCH-2 protein, C elegans

Identifiers

PMID26527744
PMCPMC4639874
OpenAlexW2143452398

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.