Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutation

Frontiers in Pharmacology

Volumn 4 OCT, Issue , 2013, Pages

  Moreau, Adrien ^a   Krahn, Andrew D ^b   Gosselin Badaroudine, Pascal ^a   Klein, George J ^c   Christé, Georges ^d   Vincent, Yohann ^d   Boutjdir, Mohamed ^e   Chahine, Mohamed ^a  

^a CENTRE DE RECHERCHE DE L INSTITUT UNIVERSITAIRE EN SANTÉ MENTALE DE QUÉBEC   (Canada)

^b UNIVERSITY OF BRITISH COLUMBIA   (Canada)

^c UNIVERSITY OF WESTERN ONTARIO   (Canada)

^d UNIVERSITÉ DE LYON   (France)

^e NEW YORK UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Cardiac arrhythmia; Electrophysiology; Heart; Long QT syndrome; LQT3; Nav1.5; Sodium overload

Indexed keywords

ARGININE; GENOMIC DNA; GLUTAMINE; SERINE; SODIUM CHANNEL NAV1.5; SODIUM ION;

ADULT; ARRHYTHMOGENESIS; ARTICLE; CELL METABOLISM; CLINICAL ARTICLE; DNA EXTRACTION; DNA SEQUENCE; EMBRYO; FAMILY STUDY; FEMALE; GAIN OF FUNCTION MUTATION; GENE; GENETIC CODE; HEART ARRHYTHMIA; HEART MUSCLE FIBER MEMBRANE POTENTIAL; HUMAN; HUMAN CELL; IN VITRO STUDY; LONG QT SYNDROME; LQT3 GENE; MALE; MOLECULAR BIOLOGY; MUTATIONAL ANALYSIS; NUCLEOTIDE SEQUENCE; PATCH CLAMP; POLYMERASE CHAIN REACTION; PROTEIN EXPRESSION; SCN5A GENE; SODIUM CURRENT; TACHYCARDIA;

EID: 84885356899     PISSN: None     EISSN: 16639812     Source Type: Journal    
DOI: 10.3389/fphar.2013.00126     Document Type: Article

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