title: Nav 1.5 mutations linked to dilated cardiomyopathy phenotypes: Is the gating pore current the missing link?
abstract: Nav 1.5 dysfunctions are commonly linked to rhythms disturbances that include type 3 long QT syndrome (LQT3), Brugada syndrome (BrS), sick sinus syndrome (SSS) and conduction defects. Recently, this channel protein has been also linked to structural heart diseases such as dilated cardiomyopathy (DCM).
authors.affiliation: Centre de recherche; Institut universitaire en santé mentale de Québec; Quebec City, QC Canada.
authors.forename: Pascal
authors.initials: P
authors.lastname: Gosselin-Badaroudine
authors.affiliation: Centre de recherche; Institut universitaire en santé mentale de Québec; Quebec City, QC Canada.
authors.forename: Adrien
authors.initials: A
authors.lastname: Moreau
authors.affiliation: Centre de recherche; Institut universitaire en santé mentale de Québec; Quebec City, QC Canada; Department of Medicine; Université Laval; Quebec City, QC Canada.
authors.forename: Mohamed
authors.initials: M
authors.lastname: Chahine
mesh_terms: D002311:Cardiomyopathy, Dilated / Q000235:genetics* / Q000503:physiopathology*; D006801:Humans; D015640:Ion Channel Gating; D009154:Mutation; D062554:NAV1.5 Voltage-Gated Sodium Channel / Q000502:physiology*; D010641:Phenotype
chemical_list: D062554:NAV1.5 Voltage-Gated Sodium Channel
keywords: Nav1.5; arrhythmias; dilated cardiomyopathy; gating pore; heart; sodium channels; structural model