Evidence map›Paper›PMID 15788770›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Deleted in colorectal cancer binding netrin-1 mediates cell substrate adhesion and recruits Cdc42, Rac1, Pak1, and N-WASP into an intracellular signaling complex that promotes growth cone expansion.

Masoud Shekarabi, Simon W Moore, Nicolas X Tritsch, Stephen J Morris, Jean-Francois Bouchard, Timothy E Kennedy

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

81 citing papers in PubMed, 170 citations in OpenAlex.

  1. Review
  2. Article
  3. Electrical Forces Improve Memory in Old Age.Reviews of physiology, biochemistry and pharmacology · 2025
    Review
  4. Article
  5. Article
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  7. NCK1 Modulates Neuronal Actin Dynamics and Promotes Dendritic Spine, Synapse, and Memory Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  8. Article
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  10. Review
  11. Article
  12. Article
  13. Review
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  15. Article
  16. Article
  17. Article
  18. Revisiting Netrin-1: One Who Guides (Axons).Frontiers in cellular neuroscience · 2018
    Review
  19. Article
  20. Building branched tissue structures: from single cell guidance to coordinated construction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review

21 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

6 authors at 2 institutions in 1 country.

Masoud ShekarabiCenter for Neuronal Survival, Montréal Neurological Institute, McGill University, Montréal, Québec, Canada H3A 2B4.
Simon W Moore
Nicolas X Tritsch
Stephen J Morris
Jean-Francois Bouchard
Timothy E Kennedy
McGill University · CAMontreal Neurological Institute and Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular cues direct axon extension by regulating growth cone morphology. The netrin-1 receptor deleted in colorectal cancer (DCC) is required for commissural axon extension to the floor plate in the embryonic spinal cord. Here we demonstrate that challenging embryonic rat spinal commissural neurons with netrin-1, either in solution or as a substrate, causes DCC-dependent increases in growth cone surface area and filopodia number, which we term growth cone expansion. We provide evidence that DCC influences growth cone morphology by at least two mechanisms. First, DCC mediates an adhesive interaction with substrate-bound netrin-1. Second, netrin-1 binding to DCC recruits an intracellular signaling complex that directs the organization of actin. We show that netrin-1-induced growth cone expansion requires Cdc42 (cell division cycle 42), Rac1 (Ras-related C3 botulinum toxin substrate 1), Pak1 (p21-activated kinase), and N-WASP (neuronal Wiskott-Aldrich syndrome protein) and that the application of netrin-1 rapidly activates Cdc42, Rac1, and Pak1. Furthermore, netrin-1 recruits Cdc42, Rac1, Pak1, and N-WASP into a complex with the intracellular domain of DCC and Nck1. These findings suggest that DCC influences growth cone morphology by acting both as a transmembrane bridge that links extracellular netrin-1 to the actin cytoskeleton and as the core of a protein complex that directs the organization of actin.

Indexed as

Analysis of VarianceAnimalsAntibodiesBlotting, Westerncdc42 GTP-Binding ProteinCells, CulturedDCC ReceptorDose-Response Relationship, DrugDrug InteractionsEmbryo, MammalianEnzyme ActivationGrowth ConesImmunohistochemistryNerve Growth FactorsNetrin-1NeuronsAntibodiescdc42 GTP-Binding ProteinDcc protein, ratDCC ReceptorNerve Growth FactorsNetrin-1Ntn1 protein, ratp21-Activated KinasesPak1 protein, ratProtein Serine-Threonine Kinasesrac1 GTP-Binding ProteinReceptors, Cell SurfaceTumor Suppressor ProteinsWas protein, ratWiskott-Aldrich Syndrome Protein

Identifiers

PMID15788770
PMCPMC6725078
OpenAlexW2090194270

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.