Evidence map›Paper›PMID 34210579›Full record

ReviewSeminars in cell & developmental biology2021

Spindle assembly checkpoint activation and silencing at kinetochores.

Pablo Lara-Gonzalez, Jonathon Pines, Arshad Desai

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 1 pooled it
18.8field-weighted citation impact, top 1% 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

151 citing papers in PubMed, 1 synthesis or guideline pooled it, 240 citations in OpenAlex.

  1. Pooled it
  2. Structure and function of the outer kinetochore.Nature reviews. Molecular cell biology · 2026
    Review
  3. Article
  4. Review
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  7. Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  8. Article
  9. Article
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  12. Expanding thebioRxiv : the preprint server for biology · 2026
    Article
  13. Article
  14. Review
  15. Article
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  18. Investigating the Consequences of Aneuploidy in Cancer and Normal Tissue.Advances in experimental medicine and biology · 2026
    Review
  19. Review
  20. Article

91 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 3 countries.

Pablo Lara-GonzalezLudwig Institute for Cancer Research, USA; Department of Cellular & Molecular Medicine, University of California San Diego, La Jolla, CA 92093, USA. Electronic address: plgonzalez@ucsd.edu.
Jonathon PinesThe Institute of Cancer Research, London, UK. Electronic address: jon.pines@icr.ac.uk.
Arshad DesaiLudwig Institute for Cancer Research, USA; Department of Cellular & Molecular Medicine, University of California San Diego, La Jolla, CA 92093, USA. Electronic address: abdesai@ucsd.edu.
Institute of Cancer Research · GBLudwig Cancer Research · BEUniversity of California San Diego · US

Funding

Kinetochore Specification and FunctionR01GM074215 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DESAI, ARSHAD · 2005 to 2025
$8.2M
Cancer Research UK C29/A24397NIGMS NIH HHS R01 GM074215Wellcome Trust
6 · The paper itself

Abstract

The spindle assembly checkpoint (SAC) is a surveillance mechanism that promotes accurate chromosome segregation in mitosis. The checkpoint senses the attachment state of kinetochores, the proteinaceous structures that assemble onto chromosomes in mitosis in order to mediate their interaction with spindle microtubules. When unattached, kinetochores generate a diffusible inhibitor that blocks the activity of the anaphase-promoting complex/cyclosome (APC/C), an E3 ubiquitin ligase required for sister chromatid separation and exit from mitosis. Work from the past decade has greatly illuminated our understanding of the mechanisms by which the diffusible inhibitor is assembled and how it inhibits the APC/C. However, less is understood about how SAC proteins are recruited to kinetochores in the absence of microtubule attachment, how the kinetochore catalyzes formation of the diffusible inhibitor, and how attachments silence the SAC at the kinetochore. Here, we summarize current understanding of the mechanisms that activate and silence the SAC at kinetochores and highlight open questions for future investigation.

Indexed as

HumansKinetochoresSpindle ApparatusAneuploidyCatalysisCheckpointChromosome segregationKinetochoresMitosis

Identifiers

PMID34210579
PMCPMC8406419
OpenAlexW3176219224

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.