Associated Papers
Effects of S906T polymorphism on the severity of a novel borderline mutation I692M in Nav 1.4 cause periodic paralysis.
Fan C et al.
Clinical Genetics, 2017
Differential thermosensitivity in mixed syndrome cardiac sodium channel mutants.
Abdelsayed M et al.
The Journal of Physiology, 2015
Channelopathies of skeletal muscle excitability.
Cannon SC
Comprehensive Physiology, 2015
Voltage-sensor movements describe slow inactivation of voltage-gated sodium channels I: wild-type skeletal muscle Na(V)1.4.
Silva JR et al.
The Journal of General Physiology, 2013
A novel mutation in SCN4A causes severe myotonia and school-age-onset paralytic episodes.
Yoshinaga H et al.
Journal of the Neurological Sciences, 2012
Skeletal muscle na channel disorders.
Simkin D et al.
Frontiers in Pharmacology, 2011
Genotype-phenotype correlation and therapeutic rationale in hyperkalemic periodic paralysis.
Jurkat-Rott K et al.
Neurotherapeutics : the Journal of the American Society for Experimental Neurotherapeutics, 2007
Human skeletal muscle sodium channelopathies.
Vicart S et al.
Neurological Sciences : Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2005
A1152D mutation of the Na+ channel causes paramyotonia congenita and emphasizes the role of DIII/S4-S5 linker in fast inactivation.
Bouhours M et al.
The Journal of Physiology, 2005
New mutations of SCN4A cause a potassium-sensitive normokalemic periodic paralysis.
Vicart S et al.
Neurology, 2004
Correlating phenotype and genotype in the periodic paralyses.
Miller TM et al.
Neurology, 2004
Impairment of slow inactivation as a common mechanism for periodic paralysis in DIIS4-S5.
Bendahhou S et al.
Neurology, 2002
Select a paper to view details