“…After the binding of Sema3A to the coreceptor complex consisting of members of the Plexin-A (PlexA) and neuropilin-1 (NRP1) families of proteins (He and Tessier-Lavigne, 1997;Kolodkin et al, 1997;Takahashi et al, 1999;Tamagnone et al, 1999), neuronal growth cones collapse as a result of the dramatic rearrangement of the actin cytoskeleton and endocytosis of the plasma membrane (Luo et al, 1993;Fournier et al, 2000;Jurney et al, 2002;Castellani et al, 2004). A role for Rho-like GTPases (Jin and Strittmatter, 1997;Zanata et al, 2002;Turner et al, 2004;Toyofuku et al, 2005), protein phosphorylation (Aizawa et al, 2001;Eickholt et al, 2002;Mitsui et al, 2002;Sasaki et al, 2002), RanBPM (Togashi et al, 2006), and members of the collapsin response mediator protein (CRMP) family (Goshima et al, 1995;Deo et al, 2004) have all been shown to play a role in Sema3A signal transduction. In addition, the intracellular molecule interacting with CasL (MICAL) has been shown to bind to PlexA receptors in Drosophila and is required for proper guidance of motor axons (Terman et al, 2002).…”