Evidence map›Paper›PMID 12684437›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Control of growth cone motility and morphology by LIM kinase and Slingshot via phosphorylation and dephosphorylation of cofilin.

Mitsuharu Endo, Kazumasa Ohashi, Yukio Sasaki, Yoshio Goshima, Ryusuke Niwa, Tadashi Uemura, Kensaku Mizuno

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

100 citing papers in PubMed, 232 citations in OpenAlex.

  1. Article
  2. Article
  3. Regulation and signaling of the LIM domain kinases.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. CryoET shows cofilactin filaments inside the microtubule lumen.bioRxiv : the preprint server for biology · 2023
    Article
  12. Review
  13. Article
  14. Inositol Polyphosphate-5-Phosphatase K (The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  15. Cofilin Signaling in the CNS Physiology and Neurodegeneration.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

40 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

7 authors at 4 institutions in 1 country.

Mitsuharu EndoDepartment of Biomolecular Sciences, Graduate School of Life Sciences, Tohoku University, Sendai 980-8578, Japan.
Kazumasa Ohashi
Yukio Sasaki
Yoshio Goshima
Ryusuke Niwa
Tadashi Uemura
Kensaku Mizuno
Tohoku University · JPYokohama City University · JPJapan Science and Technology Agency · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth cone motility and morphology are based on actin-filament dynamics. Cofilin plays an essential role for the rapid turnover of actin filaments by severing and depolymerizing them. The activity of cofilin is repressed by phosphorylation at Ser3 by LIM kinase (LIMK, in which LIM is an acronym of the three gene products Lin-11, Isl-1, and Mec-3) and is reactivated by dephosphorylation by phosphatases, termed Slingshot (SSH). We investigated the roles of cofilin, LIMK, and SSH in the growth cone motility and morphology and neurite extension by expressing fluorescence protein-labeled cofilin, LIMK1, SSH1, or their mutants in chick dorsal root ganglion (DRG) neurons and then monitoring live images of growth cones by time-lapse video fluorescence microscopy. The expression of LIMK1 remarkably repressed growth cone motility and neurite extension, whereas the expression of SSH1 or a nonphosphorylatable S3A mutant of cofilin enhanced these events. The fan-like shape of growth cones was disorganized by the expression of any of these proteins. The repressive effects on growth cone behavior by LIMK1 expression were significantly rescued by the coexpression of S3A-cofilin or SSH1. These findings suggest that LIMK1 and SSH1 play critical roles in controlling growth cone motility and morphology and neurite extension by regulating the activity of cofilin and may be involved in signaling pathways that regulate stimulus-induced growth cone guidance. Using various mutants of cofilin, we also obtained evidence that the actin-filament-severing activity of cofilin is critical for growth cone motility and neurite extension.

Indexed as

Actin CytoskeletonActin Depolymerizing FactorsAmino Acid SequenceAnimalsCells, CulturedChick EmbryoCloning, MolecularCOS CellsGanglia, SpinalGrowth ConesHeLa CellsHumansLim KinasesMicrofilament ProteinsMolecular Sequence DataMovementActin Depolymerizing FactorsLIMK1 protein, humanLim KinasesMicrofilament ProteinsPhosphoprotein PhosphatasesProtein Kinases

Identifiers

PMID12684437
PMCPMC6742113
OpenAlexW2150141558

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.