Title

DAPK activates MARK1/2 to regulate microtubule assembly, neuronal differentiation, and tau toxicity.

Journal

Cell death and differentiation

Volume

18

Issue

None

Pages

1507-20

Date

2011-09-01

Authors

Chen GC | Chen RH | Chen YH | Chien CT | Chou HJ | Huang YP | Kimchi A | Lin MY | Tsai PI | Wu PR

Furthermore, silencing of both MARK1 and MARK2 blocked DAPK-induced tau S262 phosphorylation (Figure 3e). More importantly, a decrease of pS262 tau, but not total tau, was observed in brain extracts derived from DAPK−/− mice, compared with that from DAPK+/+ mice (Figure 3f). These results strongly suggest a role of endogenous DAPK in stimulating the activity of endogenous MARK, which in turn phosphorylates tau in neurons.

Importantly, depletion of MARK1/2 reversed the inhibitory effect of DAPK on MT regrowth (Figure 5c, right panel). These results indicate that the DAPK–MARK signaling axis inhibits MT assembly and stability.

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