Key result
F1304Q mutant sodium channels exhibit prolonged open times and altered inactivation kinetics versus wild-type channels.
Population
Xenopus laevis oocytes expressing rat skeletal muscle sodium channels (mu 1) containing the F1304Q mutation
Comparison
Coexpression of the rat brain beta 1 subunit vs Without coexpression of the rat brain beta 1…
Design
Preclinical
Authors
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Cautions against clinical extrapolation from rat channels; leaves open relevance of reversible inactivation defects to human skeletal muscle channelopathies.
The F1304Q mutation in rat skeletal muscle sodium channels alters fast-inactivation kinetics, allowing reversible entry into the inactivated state independent of beta 1 subunit interactions.
Lawrence et al. (1996) studied this question. F1304Q mutation with and without coexpression of rat brain beta 1 subunit vs. Wild-type channel was evaluated on Channel gating behavior and inactivation kinetics. The F1304Q mutant sodium channels reopen multiple times with prolonged open times compared to wild-type channels, entering the inactivated state reversibly with altered kinetics.
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