Key result
The W402C mutation in domain I of the rat skeletal muscle sodium channel eliminated slow inactivation after brief depolarizations, suggesting external pore residues mediate this process.
The W402C mutation in the external pore of rat skeletal muscle sodium channels eliminates slow inactivation, suggesting that slow inactivation involves conformational changes in the external pore.
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Pore residue mutation disrupts slow Na inactivation; extends gating models but leaves open cardiac channelopathy relevance.
Balser et al. (1996) studied this question. W402C mutation in domain I vs. Wild-type alpha-subunits was evaluated on Slow inactivation after brief depolarizations. The W402C mutation in domain I of the rat skeletal muscle sodium channel eliminated slow inactivation after brief depolarizations, suggesting external pore residues mediate this process.
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