Channeling Actin Assembly in Neurons

April 8, 2016

A collaborative project between the Forscher (MCDB) and Kaczmarek (Pharmacology) labs at Yale have revealed the mechanisms by which mutations in the Kv3.3 potassium channel cause neurodegeneration.  Interestingly, the C-terminus of the channel protein recruits Arp2/3 to the plasma membrane to form a stable actin network that slows the rate of channel closing.  Mutations in the Kv3.3 channel that occur in human patients impairs Arp2/3 recruitment, resulting in defective actin networks in neuronal cells derived from human induced pluripotent stem cells.  This work highlights a novel mechanism by which the cytoskeleton regulates ion channels and provides novel targets for neuronal degeneration.

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