Wei, J <br/><br/>
Congenital long-QT syndrome caused by a novel mutation in a conserved acidic domain of the cardiac Na+ channel.  [electronic resource] 

 -  Circulation  Jun 1999 
 - 3165-71 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. 
<br/><br/><label>ISSN: </label>1524-4539 
<br/><br/><label>Standard No.: </label>10.1161/01.cir.99.24.3165  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Adolescent<br/>Animals<br/>Base Sequence<br/>Cloning, Molecular<br/>Conserved Sequence<br/>DNA Primers<br/>Death, Sudden<br/>Electrocardiography<br/>Electrophysiology<br/>Female<br/>Humans<br/>Long QT Syndrome--congenital<br/>Male<br/>Membrane Potentials--drug effects<br/>Molecular Sequence Data<br/>Mutagenesis, Site-Directed<br/>Myocardium--chemistry<br/>NAV1.5 Voltage-Gated Sodium Channel<br/>Oocytes--physiology<br/>Pedigree<br/>Point Mutation<br/>Polymorphism, Single-Stranded Conformational<br/>Protein Structure, Tertiary<br/>Sequence Homology, Amino Acid<br/>Sodium Channels--chemistry<br/>Structure-Activity Relationship<br/>Tetrodotoxin--pharmacology<br/>Xenopus