BackgroundDeoxygenation of sickle erythrocytes activates a cation permeability of unknown molecular identity (Psickle), leading to elevated intracellular [Ca2+] ([Ca2+]i) and subsequent activation of
Inherited mutations of calcium ion channels exhibit neurological defects, such as epilepsy, ataxia, and migraine, and these phenotypes are shared among humans and mouse models. Absence epilepsy and a
Brugada syndrome (BrS) is an arrhythmic disorder associated with an increased risk of sudden cardiac death; however, current treatment options are limited due to their side effects and variable effica
Objective Ataxia channelopathies share common features such as slow motor progression and variable degrees of cognitive dysfunction. Mutations in KCND3, encoding the K+ channel, Kv4.3, are associate
