Evidence map›Paper›PMID 22915102›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Netrin-1 attracts axons through FAK-dependent mechanotransduction.

Simon W Moore, Xian Zhang, Christopher D Lynch, Michael P Sheetz

Open access · bronzeAbstract readValidation Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

49 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Mechanochemistry: Fundamental Principles and Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
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  19. A Tale of Two States: Normal and Transformed, With and Without Rigidity Sensing.Annual review of cell and developmental biology · 2019
    Review
  20. Tissue mechanics, an important regulator of development and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Review
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

4 authors at 1 institution in 1 country.

Simon W MooreDepartment of Biological Sciences, Columbia University, New York, New York 10027, USA. sm3030@columbia.edu
Xian Zhang
Christopher D Lynch
Michael P Sheetz
Columbia University · US

Funding

Nanomedicine development center for mechanobiologyPN2EY016586 · NEI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DUSTIN, MICHAEL LORAN · 2005 to 2014
$23.0M
STRUCTURE AND ASSEMBLY OF CYTOSKELETAL FILAMENTSR01GM036277 · NIGMS · WASHINGTON UNIVERSITY · PI SHEETZ, MICHAEL PATRICK · 1985 to 2009
$2.8M
Mechanisms of mechanical transduction in the guidance of neuronal axonsK99NS075135 · NINDS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI MOORE, SIMON WAYNE · 2011 to 2012
$214k
CIHRNEI NIH HHS PN2 EY016586NIGMS NIH HHS 5R01GM03627NIGMS NIH HHS R01 GM036277NINDS NIH HHS 1K99NS075135NINDS NIH HHS K99 NS075135
6 · The paper itself

Abstract

The mechanism by which extracellular cues influence intracellular biochemical cascades that guide axons is important, yet poorly understood. Because of the mechanical nature of axon extension, we explored whether the physical interactions of growth cones with their guidance cues might be involved. In the context of mouse spinal commissural neuron axon attraction to netrin-1, we found that mechanical attachment of netrin-1 to the substrate was required for axon outgrowth, growth cone expansion, axon attraction and phosphorylation of focal adhesion kinase (FAK) and Crk-associated substrate (CAS). Myosin II activity was necessary for traction forces >30 pN on netrin-1. Interestingly, while these myosin II-dependent forces on netrin-1 substrates or beads were needed to increase the kinase activity and phosphorylation of FAK, they were not necessary for netrin-1 to increase CAS phosphorylation. When FAK kinase activity was inhibited, the growth cone's ability to recruit additional adhesions and to generate forces >60 pN on netrin-1 was disrupted. Together, these findings demonstrate an important role for mechanotransduction during chemoattraction to netrin-1 and that mechanical activation of FAK reinforces interactions with netrin-1 allowing greater forces to be exerted.

Indexed as

ActinsAnimalsAxonsCell Line, TransformedCrk-Associated Substrate ProteinElectroporationEmbryo, MammalianEnzyme InhibitorsEnzyme-Linked Immunosorbent AssayFemaleFocal Adhesion Protein-Tyrosine KinasesGrowth ConesHeparinHumansLuminescent ProteinsMale6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-oneActinsCrk-Associated Substrate ProteinEnzyme InhibitorsFocal Adhesion Protein-Tyrosine KinasesHeparinLuminescent ProteinsMyosin Type IINerve Growth FactorsNetrin-1NTN1 protein, humanNtn1 protein, mousePhosphoproteinsQuinolonesSulfonesTumor Suppressor ProteinsTyrosine

Identifiers

PMID22915102
PMCPMC3461192
OpenAlexW2006695366

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.