Abstract
Cheng et al (JMCC 61:102,2013) investigated the mutations in CAV3-encoding caveolin-3 (Cav3) implicated in LQT9 and SIDS. This study addressed the mechanism by which the LQT9-causing mutant Cav3-F97C affects the function of caveolar SCN5A.HEK-293 cells expressing SCN5A and Cav3-F97C resulted in a 2-fold increase in late INa versus Cav3-WT, which was reversed by the neural nitric oxide synthase (nNOS) inhibitor L-NMMA. A SCN5A macromolecular complex was established in HEK-293 cells by transiently expressing SCN5A, α1-syntrophin, nNOS, and Cav3.
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