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MOG1L18F-mediated increase in late sodium current produces Long QT Syndrome
2025-12-18
cardiovascular medicine
Title + abstract only
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BackgroundNaV1.5 channels, encoded by SCN5A, are essential for the genesis and shaping of the cardiac action potential (AP). Gain-of-function (GoF) variants in SCN5A are associated with long QT syndrome (LQTS), whereas loss-of-function (LoF) mutations are linked with Brugada syndrome. MOG1 is an integral part of the NaV1.5 channelosome, increasing both current and membrane expression of NaV1.5. Two LoF variants in MOG1 (E61X and E83D) cause Brugada Syndrome in patients, but no association with L...
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