Overexcited or inactive: Ion channels in muscle disease
- 1 March 1995
- Vol. 80 (5) , 681-686
- https://doi.org/10.1016/0092-8674(95)90345-3
Abstract
No abstract availableThis publication has 37 references indexed in Scilit:
- Purification, Reconstitution, and Subunit Composition of a Voltage-Gated Chloride Channel from Torpedo ElectroplaxBiochemistry, 1994
- Pathophysiology of sodium channelopathies: correlation of normal/mutant mRNA ratios with clinical phenotype in dominantly inherited periodic paralysisHuman Molecular Genetics, 1994
- A calcium channel mutation causing hypokalemic periodic paralysisHuman Molecular Genetics, 1994
- Proof of a non-functional muscle chloride channel in recessive myotonia congenita (Becker) by detection of a 4 base pair deletionHuman Molecular Genetics, 1994
- Dihydropyridine receptor mutations cause hypokalemic periodic paralysisCell, 1994
- Sodium channel mutations in paramyotonia congenita uncouple inactivation from activationNeuron, 1994
- Isoproterenol‐ and insulin‐induced hyperpolarization in rat skeletal muscleJournal of Cellular Physiology, 1993
- Membrane defects in paramyotonia congenita with and without myotonia in a warm environmentMuscle & Nerve, 1981
- Characteristics of the chloride conductance in muscle fibers of the rat diaphragm.The Journal of general physiology, 1977
- Destruction of Sodium Conductance Inactivation in Squid Axons Perfused with PronaseThe Journal of general physiology, 1973