Two Distinct Congenital Arrhythmias Evoked by a Multidysfunctional Na + Channel
- 12 May 2000
- journal article
- other
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 86 (9) , E91-7
- https://doi.org/10.1161/01.res.86.9.e91
Abstract
—The congenital long-QT syndrome (LQT3) and the Brugada syndrome are distinct, life-threatening rhythm disorders linked to autosomal dominant mutations in SCN5A, the gene encoding the human...Keywords
This publication has 21 references indexed in Scilit:
- Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome: A multicenter reportPublished by Elsevier ,2010
- Molecular Dynamics of the Sodium Channel Pore Vary with Gating: Interactions between P-Segment Motions and InactivationJournal of Neuroscience, 1999
- Drug-Induced J Point Elevation.Journal of Cardiovascular Electrophysiology, 1999
- Genetic basis and molecular mechanism for idiopathic ventricular fibrillationNature, 1998
- Characterization of human cardiac Na + channel mutations in the congenital long QT syndromeProceedings of the National Academy of Sciences, 1996
- Paramyotonia congenita mutations reveal different roles for segments S3 and S4 of domain D4 in hSkM1 sodium channel gating.The Journal of general physiology, 1996
- Molecular mechanism for an inherited cardiac arrhythmiaNature, 1995
- Evidence for voltage-dependent S4 movement in sodium channelsNeuron, 1995
- SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndromeCell, 1995
- A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation.Proceedings of the National Academy of Sciences, 1992