| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8473915 | Journal of Molecular and Cellular Cardiology | 2016 | 35 Pages |
Abstract
The p.R1309H homozygous NaV1.5 mutation conferred both gain-of-function and loss-of-function effects on NaV1.5 channel activity. Reduction of a mutation-induced gating pore current by lidocaine suggested a therapeutic mechanism.
Keywords
AEDVCFNav1.5VSDeGFPHEKAutomated external defibrillatorsArginineVentricular arrhythmiaAtrial arrhythmiaCardiopulmonary resuscitationCPRECGelectrocardiogramTryptophanTyrosineSerineVoltage sensorCysteineMethioninewild typehistidineenhanced green fluorescent proteinsodium channelshuman embryonic kidneyglutamine
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Authors
Hong-Gang Wang, Wandi Zhu, Ronald J. Kanter, Jonathan R. Silva, Christina Honeywell, Robert M. Gow, Geoffrey S. Pitt,