Evidence map›Paper›PMID 23512483›Full record

ReviewChromosoma2013

Making an effective switch at the kinetochore by phosphorylation and dephosphorylation.

Hironori Funabiki, David J Wynne

Open access · greenAbstract readReview
In one paragraph

Review in Chromosoma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
9.9field-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

76 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Science advances · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Hec1/Ndc80 Tail Domain Function at the Kinetochore-Microtubule Interface.Frontiers in cell and developmental biology · 2020
    Review
  20. Article

16 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

2 authors at 1 institution in 1 country.

Hironori FunabikiLaboratory of Chromosome and Cell Biology, The Rockefeller University, 1230 York Avenue, New York, NY, 10065, USA. funabih@rockefeller.edu
David J Wynne
Rockefeller University · US

Funding

Roles of Chromosomal Factors in Chromosome SegregationR01GM075249 · NIGMS · ROCKEFELLER UNIVERSITY · PI FUNABIKI, HIRONORI · 2005 to 2018
$4.5M
Determining how the spindle assembly checkpoint monitors chromosome biorientationF32GM103147 · NIGMS · ROCKEFELLER UNIVERSITY · PI WYNNE, DAVID J · 2012 to 2013
$106k
NIGMS NIH HHS 1F32GM103147NIGMS NIH HHS F32 GM103147NIGMS NIH HHS R01 GM075249NIGMS NIH HHS R01GM075249
6 · The paper itself

Abstract

The kinetochore, the proteinaceous structure on the mitotic centromere, functions as a mechanical latch that hooks onto microtubules to support directional movement of chromosomes. The structure also brings in a number of signaling molecules, such as kinases and phosphatases, which regulate microtubule dynamics and cell cycle progression. Erroneous microtubule attachment is destabilized by Aurora B-mediated phosphorylation of multiple microtubule-binding protein complexes at the kinetochore, such as the KMN network proteins and the Ska/Dam1 complex, while Plk-dependent phosphorylation of BubR1 stabilizes kinetochore-microtubule attachment by recruiting PP2A-B56. Spindle assembly checkpoint (SAC) signaling, which is activated by unattached kinetochores and inhibits the metaphase-to-anaphase transition, depends on kinetochore recruitment of the kinase Bub1 through Mps1-mediated phosphorylation of the kinetochore protein KNL1 (also known as Blinkin in mammals, Spc105 in budding yeast, and Spc7 in fission yeast). Recruitment of protein phosphatase 1 to KNL1 is necessary to silence the SAC upon bioriented microtubule attachment. One of the key unsolved questions in the mitosis field is how a mechanical change at the kinetochore upon microtubule attachment is converted to these and other chemical signals that control microtubule attachment and the SAC. Rapid progress in the field is revealing the existence of an intricate signaling network created right on the kinetochore. Here we review the current understanding of phosphorylation-mediated regulation of kinetochore functions and discuss how this signaling network generates an accurate switch that turns on and off the signaling output in response to kinetochore-microtubule attachment.

Indexed as

MitosisPhosphorylationAnimalsChromosome SegregationHumansKinetochoresMicrotubulesProtein BindingSaccharomycetalesSpindle Apparatus

Identifiers

PMID23512483
PMCPMC3665160
OpenAlexW1987832868

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.