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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 bimodal inactivation, with two gating modes that inactivate with time constants that differ at least by one order of...

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Source

Identifiers

PMID: 9618291
DOI: 10.1006/bbrc.1998.8718

Genes

PAM

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Inactivation defects produced by a myopathic II-S6 mutation of the muscle sodium channel.PMID 9618291Read ↗

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