8 research outputs found
Protein Kinase CĪµ Actin-binding Site Is Important for Neurite Outgrowth during Neuronal Differentiation
We have previously shown that protein kinase CĪµ (PKCĪµ) induces neurite outgrowth via its regulatory domain and independently of its kinase activity. This study aimed at identifying mechanisms regulating PKCĪµ-mediated neurite induction. We show an increased association of PKCĪµ to the cytoskeleton during neuronal differentiation. Furthermore, neurite induction by overexpression of full-length PKCĪµ is suppressed if serum is removed from the cultures or if an actin-binding site is deleted from the protein. A peptide corresponding to the PKCĪµ actin-binding site suppresses neurite outgrowth during neuronal differentiation and outgrowth elicited by PKCĪµ overexpression. Neither serum removal, deletion of the actin-binding site, nor introduction of the peptide affects neurite induction by the isolated regulatory domain. Membrane targeting by myristoylation renders full-length PKCĪµ independent of both serum and the actin-binding site, and PKCĪµ colocalized with F-actin at the cortical cytoskeleton during neurite outgrowth. These results demonstrate that the actin-binding site is of importance for signals acting on PKCĪµ in a pathway leading to neurite outgrowth. Localization of PKCĪµ to the plasma membrane and/or the cortical cytoskeleton is conceivably important for its effect on neurite outgrowth