Cargando…
Domain III S4 in closed-state fast inactivation: Insights from a periodic paralysis mutation
Heterologous expression of sodium channel mutations in hypokalemic periodic paralysis reveals 2 variants on channel dysfunction. Charge-reducing mutations of voltage sensing S4 arginine residues alter channel gating as typically studied with expression in mammalian cells. These mutations also produc...
Autores principales: | Groome, James R, Jurkat-Rott, Karin, Lehmann-Horn, Frank |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2014
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594372/ https://www.ncbi.nlm.nih.gov/pubmed/25483590 http://dx.doi.org/10.4161/19336950.2014.958924 |
Ejemplares similares
-
Na(V)1.4 mutations cause hypokalaemic periodic paralysis by disrupting IIIS4 movement during recovery
por: Groome, James R., et al.
Publicado: (2014) -
Na(V)1.4 DI-S4 periodic paralysis mutation R222W enhances inactivation and promotes leak current to attenuate action potentials and depolarize muscle fibers
por: Bayless-Edwards, Landon, et al.
Publicado: (2018) -
Do Hyperpolarization-induced Proton Currents Contribute to the Pathogenesis of Hypokalemic Periodic Paralysis, a Voltage Sensor Channelopathy?
por: Jurkat-Rott, Karin, et al.
Publicado: (2007) -
Transient compartment-like syndrome and normokalaemic periodic paralysis due to a Ca(v)1.1 mutation
por: Fan, Chunxiang, et al.
Publicado: (2013) -
Rare KCNJ18 variants do not explain hypokalaemic periodic paralysis in 263 unrelated patients
por: Kuhn, Marius, et al.
Publicado: (2016)