Abstract
Human Ether-a-go-go-Related Gene (hERG) encodes a potassium-selective voltage-gated ion channel essential for normal electrical activity in the heart. Genetic hERG mutations and blockage of the channel pore by drugs can cause long QT syndrome (LQTS). LQTS predisposes individuals to arrhythmia and puts them at risk for stroke or sudden cardiac arrest. A major problem in antiarrhythmic drug therapies is the proclivity for these drugs to promote fatal arrhythmias through hERG channel blockade. However, not all hERG channel blocking drugs are pro-arrhythmic, and their differential affinities to discrete channel conformational states and/or their state stability modulations have been suggested to contribute to arrhythmogenicity.
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