Evidence map›Paper›PMID 10066250›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Myelin and collapsin-1 induce motor neuron growth cone collapse through different pathways: inhibition of collapse by opposing mutants of rac1.

T B Kuhn, M D Brown, C L Wilcox, J A Raper, J R Bamburg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 185 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Review
  6. Structural mechanisms of plexin signaling.Progress in biophysics and molecular biology · 2015
    Review
  7. Article
  8. Article
  9. Review
  10. Article
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  12. Article
  13. Atypical protein kinase C and Par3 are required for proteoglycan-induced axon growth inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Rho GTPases as regulators of morphological neuroplasticity.Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft · 2011
    Review
  19. Anti-ganglioside antibody-mediated activation of RhoA induces inhibition of neurite outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  20. Review

2 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

5 authors at 3 institutions in 2 countries.

T B KuhnDepartment of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523, USA.
M D Brown
C L Wilcox
J A Raper
J R Bamburg
Colorado State University · USInstitute of Neurobiology · BGUniversity of Pennsylvania · US

Funding

STRUCTURE/FUNCTION OF ACTIN DEPOLYMERIZING FACTORR01GM035126 · NIGMS · COLORADO STATE UNIVERSITY-FORT COLLINS · PI BAMBURG, JAMES R · 1985 to 2003
$1.1M
NIGMS NIH HHS GM35126NIGMS NIH HHS GM54005NIGMS NIH HHS R01 GM035126
6 · The paper itself

Abstract

Precise growth cone guidance is the consequence of a continuous reorganization of actin filament structures within filopodia and lamellipodia in response to inhibitory and promoting cues. The small GTPases rac1, cdc42, and rhoA are critical for regulating distinct actin structures in non-neuronal cells and presumably in growth cones. Collapse, a retraction of filopodia and lamellipodia, is a typical growth cone behavior on contact with inhibitory cues and is associated with depolymerization and redistribution of actin filaments. We examined whether small GTPases mediate the inhibitory properties of CNS myelin or collapsin-1, a soluble semaphorin, in chick embryonic motor neuron cultures. As demonstrated for collapsin-1, CNS myelin-evoked growth cone collapse was accompanied by a reduction of rhodamine-phalloidin staining most prominent in the growth cone periphery, suggesting actin filament disassembly. Specific mutants of small GTPases were capable of desensitizing growth cones to CNS myelin or collapsin-1. Adenoviral-mediated expression of constitutively active rac1 or rhoA abolished CNS myelin-induced collapse and allowed remarkable neurite extension on a CNS myelin substrate. In contrast, expression of dominant negative rac1 or cdc42 negated collapsin-1-induced growth cone collapse and promoted neurite outgrowth on a collapsin-1 substrate. These findings suggest that small GTPases can modulate the signaling pathways of inhibitory stimuli and, consequently, allow the manipulation of growth cone behavior. However, the fact that opposite mutants of rac1 were effective against different inhibitory stimuli speaks against a universal signaling pathway underlying growth cone collapse.

Indexed as

ActinsAdenoviridaeAnimalscdc42 GTP-Binding ProteinCell Cycle ProteinsCells, CulturedCentral Nervous SystemChick EmbryoGenetic VectorsGlycoproteinsGrowth ConesGTP-Binding ProteinsGTP PhosphohydrolasesMotor NeuronsMutationMyelin SheathActinscdc42 GTP-Binding ProteinCell Cycle ProteinsGlycoproteinsGTP-Binding ProteinsGTP Phosphohydrolasesrac GTP-Binding ProteinsrhoA GTP-Binding ProteinSemaphorin-3A

Identifiers

PMID10066250
PMCPMC6782563
OpenAlexW1646460047

What OpenQuestion holds

Texttitle and abstract
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.