Article
MOG1 rescues defective trafficking of Na(v)1.5 mutations in Brugada syndrome and sick sinus syndrome.
Circulation. Arrhythmia and electrophysiology - 1 Apr 2013
Chakrabarti Susmita, Wu Xiaofen, Yang Zhaogang, Wu Ling, Yong Sandro L, Zhang Cuntai, Hu Keli, Wang Qing K, Chen Qiuyun
Abstract excerpt
BACKGROUND: Loss-of-function mutations in Na(v)1.5 cause sodium channelopathies, including Brugada syndrome, dilated cardiomyopathy, and sick sinus syndrome; however, no effective therapy exists. MOG1 increases plasma membrane (PM) expression of Na(v)1.5 and sodium current (I(Na)) density, thus we hypothesize that MOG1 can serve as a therapeutic target for sodium channelopathies. METHODS AND RESULTS: Knockdown of...
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