Key result
S4-S5 and S6 mutations eliminate slow off-gating in Shaker K+ channels by impairing intersubunit interactions.
Identifies a specific intersubunit interaction responsible for the slow off-gating component and open-state stabilization in Shaker K+ channels.
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Identifies residues mediating slow off-gating in Shaker K+ channels; extends mechanistic models of voltage-gated K+ gating but leaves clinical translation open.
Batulan et al. (2010) studied this question. Mutation of residues Arg-394, Glu-395, Leu-398, and Tyr-485 vs. Wild-type channels was evaluated on Slow off-gating component and gating kinetics. Mutation of specific residues on the S4-S5 linker and S6 impaired intersubunit interactions, leading to pore opening without the slow off-gating component in Shaker K+ channels.
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