Abstract
The neural cell adhesion molecule (NCAM) can regulate actin cytoskeletal dynamics through associations with growth-associated protein-43 (GAP-43). By binding to the fibroblast growth factor receptor (FGFR), NCAM activates intracellular pathways to trigger calcium release, lipid diacylglycerol (DAG) formation, and protein kinase C (PKC) activation to specifically phosphorylate GAP-43 on serine 41. Phosphorylated GAP-43 plays a key role in neurite outgrowth, presumably by promoting actin polymerization. Of all NCAM isoforms, only NCAM-180 takes part in this GAP-43-dependent neurite outgrowth. GAP-43 and NCAM-180 are found in the same plasma membrane domains (rafts), and these two proteins form a functional complex with spectrin that may control cytoskeleton dynamics to induce neurite outgrowth. In the absence of GAP-43, the signaling pathway that depends on NCAM-140 and nonreceptor tyrosine kinase (Fyn) is activated.
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