This is a brief review of the mechanism of laminin-mediated neurite outgrowth in which several key observations are presented with the purpose of developing a model of the key molecular events involved with laminin active site interaction with receptors, signal transduction, cytoskeletal rearrangement, basement membrane remodeling and growth cone extension. This is a thorough review of the known laminin active sites, receptors, signal transduction pathways and alteration in gene expression. However, this review is not designed as a catalog of these events. Instead, this review is designed to link the simultaneous role of laminin both as an adhesion molecule for neurons and as a malleable substrate that growth cones can detach from and move along. Underlying this apparent contradictory function, simultaneous stabilization and destabilization of the cytoskeleton is required for neurite elongation. Here, a model of the mechanism of laminin-mediated neurite outgrowth is developed that illustrates the structural, architectural and biochemical sequence that leads to laminin-mediated neurite outgrowth.
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