A defect in skeletal muscle sodium channel deactivation exacerbates hyperexcitability in human paramyotonia congenita

Journal of Physiology

Volumn 506, Issue 3, 1998, Pages 627-638

  Featherstone, David E ^a,b   Fujimoto, Esther ^a   Ruben, Peter C ^a  

^a UTAH STATE UNIVERSITY   (United States)

^b UNIVERSITY OF UTAH   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

MUTANT PROTEIN; SODIUM CHANNEL; SODIUM ION; VOLTAGE GATED CHANNEL FORMING PROTEIN; ARGININE; CYSTEINE; PROLINE; SODIUM;

AMINO ACID SUBSTITUTION; ANIMAL CELL; ARTICLE; CONTROLLED STUDY; HUMAN; MISSENSE MUTATION; MUSCLE ACTION POTENTIAL; MUSCLE EXCITATION; NONHUMAN; PRIORITY JOURNAL; RAT; SKELETAL MUSCLE; SODIUM CURRENT; THOMSEN DISEASE; ANIMAL TISSUE; CHANNEL GATING; DISEASE EXACERBATION; DISEASE SEVERITY; ELECTRIC POTENTIAL; PATHOGENESIS; PREDICTION; PROTEIN DOMAIN; REPOLARIZATION; TEMPERATURE SENSITIVITY; WILD TYPE;

ACTION POTENTIALS; ANIMALS; ELECTRIC STIMULATION; ELECTROPHYSIOLOGY; ION CHANNEL GATING; MEMBRANE POTENTIALS; MUSCLE, SKELETAL; MUTAGENESIS, SITE-DIRECTED; MYOTONIA CONGENITA; PATCH-CLAMP TECHNIQUES; RATS; SODIUM CHANNELS; TEMPERATURE; TRANSCRIPTION, GENETIC;

EID: 0032007991     PISSN: 00223751     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1469-7793.1998.627bv.x     Document Type: Article

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