Evidence map›Paper›PMID 19135897›Full record

ArticleCell2009

The mechanism of Ca2+ -dependent regulation of kinesin-mediated mitochondrial motility.

Xinnan Wang, Thomas L Schwarz

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 528 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
528citing papers in PubMed, 2 pooled it
24.6field-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

528 citing papers in PubMed, 2 syntheses or guidelines pooled it, 874 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  4. Review
  5. Mitochondrial molecular diversity in the brain.Current opinion in neurobiology · 2026
    Review
  6. Review
  7. The KIF6-RBP Complex Orchestrates mRNA Transport Required for Sperm Flagellar Assembly.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The MIRO1-BAX Complex Dictates Life and Death at the Mitochondrial Gate.bioRxiv : the preprint server for biology · 2026
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Motor-Assisted Co-Migration of Intracellular Organelles and Microtubules as a Mechanism for Directed Cargo Transport.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  19. Review
  20. Article

468 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.

Xinnan WangF.M. Kirby Neurobiology Center, Children's Hospital Boston, Boston, MA 02115, USA.
Thomas L Schwarz
Boston Children's Hospital · US

Funding

Milton/Trak 1/2 Protein and the Transport of MitochondriaR01GM069808 · NIGMS · CHILDREN'S HOSPITAL BOSTON · PI SCHWARZ, THOMAS L. · 2004 to 2022
$5.2M
NIGMS NIH HHS R01 GM069808NIGMS NIH HHS R01GM069808
6 · The paper itself

Abstract

Mitochondria are mobile organelles and cells regulate mitochondrial movement in order to meet the changing energy needs of each cellular region. Ca(2+) signaling, which halts both anterograde and retrograde mitochondrial motion, serves as one regulatory input. Anterograde mitochondrial movement is generated by kinesin-1, which interacts with the mitochondrial protein Miro through an adaptor protein, milton. We show that kinesin is present on all axonal mitochondria, including those that are stationary or moving retrograde. We also show that the EF-hand motifs of Miro mediate Ca(2+)-dependent arrest of mitochondria and elucidate the regulatory mechanism. Rather than dissociating kinesin-1 from mitochondria, Ca(2+)-binding permits Miro to interact directly with the motor domain of kinesin-1, preventing motor/microtubule interactions. Thus, kinesin-1 switches from an active state in which it is bound to Miro only via milton, to an inactive state in which direct binding to Miro prevents its interaction with microtubules. Disrupting Ca(2+)-dependent regulation diminishes neuronal resistance to excitotoxicity.

Indexed as

AnimalsCalciumCell LineCells, CulturedHippocampusHumansKinesinsMicrotubulesMitochondriaMitochondrial ProteinsNerve Tissue ProteinsNeuronsRatsCalciumKinesinsMitochondrial ProteinsNerve Tissue Proteins

Identifiers

PMID19135897
PMCPMC2768392
OpenAlexW1996764498

What OpenQuestion 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 OpenQuestion graph.