Abstract
The potassium channel KV11.1 plays an important role in repolarization of cardiac action potentials and loss-of-function (LOF) KV11.1 variants cause Long QT Syndrome which predisposes individuals to fatal cardiac arrhythmias. About 90% of LOF mutations prevent KV11.1 intracellular transport (trafficking) to the plasma membrane and prolonged incubation with drugs can sometimes increase KV11.1 trafficking and restore KV11.1 current (IKr).
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