Inactivation defects caused by myotonia-associated mutations in the sodium channel III-IV linker

Journal of General Physiology

Volumn 107, Issue 5, 1996, Pages 559-576

  Hayward, Lawrence J ^a   Brown Jr , Robert H ^a   Cannon, Stephen C ^a,b  

^a MASSACHUSETTS GENERAL HOSPITAL   (United States)

^b HARVARD MEDICAL SCHOOL   (United States)

Author keywords

familial; human; ion channels; muscle; paralysis

Indexed keywords

SODIUM CHANNEL;

ANIMAL CELL; ANIMAL TISSUE; ARTICLE; MISSENSE MUTATION; MYOTONIA; NONHUMAN; PATHOPHYSIOLOGY; RAT; SKELETAL MUSCLE; SODIUM CURRENT;

ANIMALS; CELL MEMBRANE PERMEABILITY; CELLS, CULTURED; ELECTROPHYSIOLOGY; HUMANS; KINETICS; MODELS, BIOLOGICAL; MUSCLE, SKELETAL; MUTAGENESIS, SITE-DIRECTED; MUTATION; MYOTONIA; PATCH-CLAMP TECHNIQUES; PHENOTYPE; RATS; SODIUM CHANNELS; TEMPERATURE; TRANSFECTION;

EID: 0029926886     PISSN: 00221295     EISSN: None     Source Type: Journal    
DOI: 10.1085/jgp.107.5.559     Document Type: Article

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