A substantial body of evidence indicates that protein kinase C (PKC) is involved
in the alpha-secretory processing of the amyloid precursor protein (APP), an
event that reduces the formation of the pathogenic amyloid-beta peptide.
Recently, we have shown that trafficking and processing of APP are both impaired
by knockdown of myosin II-B, one of the major neuronal motor proteins. Here, we
provide evidence that the alpha-secretory processing of APP is mediated by
PKC-dependent phosphorylation of myosin II-B. This signaling pathway provides an
important link between APP and the neuronal cytoskeleton and might be crucial for
the understanding of the biological and pathological roles of APP
