c-jun N-terminal kinase hyperphosphorylates R406W tau at the PHF-1 site during mitosis.

Presents a study which investigated the mechanisms of PHF-1 hyperphosphorylation of tau with a FTDP17 mutation R406W that causes Alzheimer disease-like dementia and taupathy in humans but has a unique ability to reduce tau phosphorylation at the PHF-1 site in vitro and in cultured cells. Inhibition of tau phosphorylation at Ser404 by the R406W mutation; Involvement of JNK in the phosphorylation of R406W tau at the PHF-1 site.