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The voltage-gated potassium channel subunit Kv11.1, encoded by the KCNH2 gene, forms the pore-forming alpha subunit of the hERG channel, a member of the voltage-gated potassium channel family.[1][4][3] The channel plays a critical role in the electrical repolarization of cardiac muscle after each heartbeat by mediating the rapid delayed rectifier potassium current (I_Kr), essential for maintaining a regular heart rhythm.[3][4] Each channel consists of four identical subunits with six transmembrane segments and specialized intracellular domains. Blockade or genetic mutation of Kv11.1/hERG can cause the dangerous arrhythmia "long QT syndrome," and many drugs withdrawn from the market have shown unintended hERG blockade. Beyond cardiology, KCNH2/hERG is expressed in neurons and some immune cells, and has been implicated in certain cancer cell phenotypes.[1][2][3][4]
Blockade of the Kv11.1 (hERG) channel inhibits the IKr current, leading to prolonged repolarization phase of the cardiac action potential (lengthened QT interval). Some drugs interact as open-channel blockers. Channel agonists (less common, mainly experimental).
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