The episodic ataxia type-1-associated V408A mutation impairs Kv1.1 channel function by destabilizing the open conformation of the activation gate rather than through C-type inactivation.
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Refines episodic ataxia type-1 mechanism to activation-gate destabilization; challenges C-type inactivation model and leaves open targeted therapies.
Peters et al. (2011) studied this question.
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