Inactivation defects produced by a myopathic II-S6 mutation of the muscle sodium channel.

doi:10.1006/bbrc.1998.8718

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Article

Inactivation defects produced by a myopathic II-S6 mutation of the muscle sodium channel.

Biochemical and biophysical research communications - 29 May 1998

Moran O, Nizzari M, Conti F

Abstract excerpt

We have studied the expression in frog oocytes of the alpha-subunit of the rat skeletal muscle sodium channel mutation S798F, homologous to the mutation S804F of the human isoform, that causes potassium aggravated myotony (PAM), a muscular hereditary disease in humans. Wild type channels show a b...

Topics

Animals
Electrophysiology
Ion Channel Gating
Muscle Proteins
Muscle, Skeletal
Mutation
Myotonia
Potassium
Rats
Recombinant Proteins
Sodium Channels

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