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Rac3-induced neuritogenesis requires binding to Neurabin I.

Authors: Orioli, D  Colaluca, IN  Stefanini, M  Riva, S  Dotti, CG  Peverali, FA 
Citation: Orioli D, etal., Mol Biol Cell. 2006 May;17(5):2391-400. Epub 2006 Mar 8.
Pubmed: (View Article at PubMed) PMID:16525025
DOI: Full-text: DOI:10.1091/mbc.E05-08-0753

Rac3, a neuronal GTP-binding protein of the Rho family, induces neuritogenesis in primary neurons. Using yeast two-hybrid analysis, we show that Neurabin I, the neuronal F-actin binding protein, is a direct Rac3-interacting molecule. Biochemical and light microscopy studies indicate that Neurabin I copartitions and colocalizes with Rac3 at the growth cones of neurites, inducing Neurabin I association to the cytoskeleton. Moreover, Neurabin I antisense oligonucleotides abolish Rac3-induced neuritogenesis, which in turn is rescued by exogenous Neurabin I but not by Neurabin I mutant lacking the Rac3-binding domain. These results show that Neurabin I mediates Rac3-induced neuritogenesis, possibly by anchoring Rac3 to growth cone F-actin.


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CRRD Object Information
CRRD ID: 8554233
Created: 2014-05-08
Species: All species
Last Modified: 2014-05-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.