Conventional kinesin (kinesin-1, KIF5) is a plus-end microtubule-based motor, and defects in kinesin-based transport are linked to neurodegeneration. Kinesin can auto-inhibit via a direct head-tail interaction, but is believed to be active otherwise. In contrast, we report here a tail-independent inactivation of kinesin, reversible by the disease-relevant signaling protein, casein kinase 2. While we identified this novel regulation pathway in vitro, we confirm its relevance in cells. These results provide the first direct evidence of a protein kinase up-regulating kinesin-transport, and suggest a novel pathway via which activity of cargo-bound kinesin can be regulated.
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