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Pyk2 and FAK regulate neurite outgrowth induced by growth factors and integrins.

Authors: Ivankovic-Dikic, I  Gronroos, E  Blaukat, A  Barth, BU  Dikic, I 
Citation: Ivankovic-Dikic I, etal., Nat Cell Biol. 2000 Sep;2(9):574-81.
Pubmed: (View Article at PubMed) PMID:10980697
DOI: Full-text: DOI:10.1038/35023515

Integration of signalling pathways initiated by receptor tyrosine kinases and integrins is essential for growth-factor-mediated biological responses. Here we show that co-stimulation of growth-factor receptors and integrins activates the focal-adhesion kinase (FAK) family to promote outgrowth of neurites in PC12 and SH-SY5Y cells. Pyk2 and FAK associate with adhesion-based complexes that contain epidermal growth factor (EGF) receptors, through their carboxy- and amino-terminal domains. Expression of the C-terminal domain of Pyk2 or of FAK is sufficient to block neurite outgrowth, but not activation of extracellular-signal-regulated kinase (ERK). Moreover, activation and autophosphorylation of Pyk2/FAK, as well as of effectors of their adhesion-targeting domains, such as paxillin, are important for propagation of signals that control neurite formation. Thus, Pyk2/FAK have important functions in signal integration proximal to integrin/growth-factor receptor complexes in neurons.


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CRRD Object Information
CRRD ID: 1642629
Created: 2007-10-04
Species: All species
Last Modified: 2007-10-04
Status: ACTIVE


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