Overexcited or inactive: Ion channels in muscle disease

Cell

Volumn 80, Issue 5, 1995, Pages 681-686

  Hoffman, Eric P ^a   Lehmann Horn, Frank ^b   Rädel, Reinhardt ^b  

^a Departments of Molecular Genetics and Biochemistry Human Genetics Pediatrics University ^*  (United States)

^b UNIVERSITY OF ULM   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM; CALCIUM CHANNEL; CHLORIDE CHANNEL; DIHYDROPYRIDINE; POTASSIUM; SODIUM; SODIUM CHANNEL;

AMINO ACID SUBSTITUTION; CALCIUM CURRENT; CHLORIDE CONDUCTANCE; GENE MUTATION; GENETIC LINKAGE; HUMAN; MUSCLE DISEASE; MYOTONIA; NONHUMAN; PERIODIC PARALYSIS; PRIORITY JOURNAL; REVIEW; THOMSEN DISEASE; VOLTAGE CLAMP;

EID: 0028913998     PISSN: 00928674     EISSN: None     Source Type: Journal    
DOI: 10.1016/0092-8674(95)90345-3     Document Type: Review

References (41)

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12. A calcium channel mutation causing hypokalemic periodic paralysis
13. Linkage data suggesting allelic heterogeneity for paramyotonia congenita and hyperkalemic periodic paralysis
14. Tight linkage of recessive and dominant forms of human myotonia to skeletal muscle chloride channel gene
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17. Altered calcium currents in human hypokalemic periodic paralysis myotubes expressing mutant L-type calcium channels
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19. Isoproterenol-and insulin-induced hyperpolarization in rat skeletal muscle
20. Cable parameters, sodium, potassium, chloride, and water content and potassium efflux in isolated external intercostal muscle of normal volunteers and patients with myotonia congenita
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27. Paramyotonia congenita and hyperkalemic periodic paralysis map to the same sodium channel gene locus
28. Identification of a mutation in the gene causing hyperkalemic periodic paralysis
29. Dihydropyridine receptor mutations cause hypokalemic periodic paralysis
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40. + channel inactivation
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