Evidence map›Paper›PMID 19851335›Full record

ReviewNature reviews. Molecular cell biology2009

Traffic control: regulation of kinesin motors.

Kristen J Verhey, Jennetta W Hammond

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Molecular cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 301 papers.

0numbers the graph read from it
0cells of the map it votes in
301citing papers in PubMed
11.5field-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

301 citing papers in PubMed, 560 citations in OpenAlex.

  1. The KIF6-RBP Complex Orchestrates mRNA Transport Required for Sperm Flagellar Assembly.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
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  5. CLASP2 promotes repair of kinesin-1 damage to the microtubule lattice.bioRxiv : the preprint server for biology · 2026
    Article
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  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Joubert syndrome 26 protein enforces compartmentalized motility of a ciliary kinesin.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Article
  18. New variants and genotype-phenotype correlation inJournal of medical genetics · 2025
    Article
  19. Article
  20. Review

241 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.

Kristen J VerheyDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan 48109-2200, USA. kjverhey@umich.edu
Jennetta W Hammond
University of Michigan–Ann Arbor · US

Funding

Regulation of the molecular motor kinesin-IR01GM070862 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI VERHEY, KRISTEN J. · 2005 to 2018
$4.2M
NIGMS NIH HHS R01 GM070862
6 · The paper itself

Abstract

Kinesins are a family of molecular motors that use the energy of ATP hydrolysis to move along the surface of, or destabilize, microtubule filaments. Much progress has been made in understanding the mechanics and functions of the kinesin motors that play important parts in cell division, cell motility, intracellular trafficking and ciliary function. How kinesins are regulated in cells to ensure the temporal and spatial fidelity of their microtubule-based activities is less well understood. Recent work has revealed molecular mechanisms that control kinesin autoinhibition and subsequent activation, binding to cargos and microtubule tracks, and localization at specific sites of action.

Indexed as

AnimalsHumansKinesinsMicrotubulesSpindle ApparatusKinesins

Identifiers

PMID19851335
OpenAlexW1996637041

What OpenQuestion holds

Textmetadata
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.