Changes in action potentials and intracellular ionic homeostasis in a ventricular cell model related to a persistent sodium current in SCN5A mutations underlying LQT3

Progress in Biophysics and Molecular Biology

Volumn 96, Issue 1-3, 2008, Pages 281-293

  Christe G ^a   Chahine, M ^b   Chevalier, P ^c   Pasek M ^d,e  

^a INSERM   (France)

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

^c LOUIS PRADEL HOSPITAL   (France)

^d INSTITUTE OF THERMOMECHANICS   (Czech Republic)

^e MASARYK UNIVERSITY   (Czech Republic)

Author keywords

Long QT syndrome; Model; Mutation; SCN5A; Sudden death

Indexed keywords

SODIUM; SODIUM CHANNEL; VOLTAGE GATED NA+ CHANNEL NA(V)1.5A; VOLTAGE-GATED NA+ CHANNEL NA(V)1.5A;

ACTION POTENTIAL; ANIMAL; BIOLOGICAL MODEL; COMPARATIVE STUDY; CYTOLOGY; GENETICS; HEART MUSCLE CELL; HEART VENTRICLE; HOMEOSTASIS; HUMAN; INTRACELLULAR FLUID; LONG QT SYNDROME; METABOLISM; MUTATION; PHYSIOLOGY; REVIEW;

ACTION POTENTIALS; ANIMALS; HEART VENTRICLES; HOMEOSTASIS; HUMANS; INTRACELLULAR FLUID; LONG QT SYNDROME; MODELS, CARDIOVASCULAR; MUTATION; MYOCYTES, CARDIAC; SODIUM; SODIUM CHANNELS;

CAVIA;

EID: 43049168662     PISSN: 00796107     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.pbiomolbio.2007.07.023     Document Type: Review

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