Human ether-à-go-go-related gene potassium channel (hERG) and Inward rectifier potassium channel 1 (I_K1) (hERG (KCNH2, Kv11.1) and Kir2.1 (KCNJ2; for I_K1))

The **human ether-à-go-go-related gene potassium channel (hERG, Kv11.1; encoded by KCNH2)** is a voltage-gated potassium channel that forms the pore for the rapid delayed rectifier K⁺ current (I_Kr) in cardiac myocytes, essential for repolarization of the ventricular action potential and thus for proper electrical conduction in the heart[1][5][10]. hERG’s structure features six transmembrane segments per subunit (S1–S6), with a voltage-sensing domain and a selective pore, forming a tetrameric channel with unique gating and inactivation kinetics critical for cardiac rhythm[1][10]. The channel's pharmacological promiscuity leads to frequent unintended blockade by a wide range of drugs, which can precipitate drug-induced long QT syndrome and life-threatening arrhythmias, hence its central role in drug safety testing[1][5][10]. The **inward rectifier potassium channel 1 (I_K1; typically formed by Kir2.1 encoded by KCNJ2)** contributes to maintaining the cardiac resting membrane potential and late phase repolarization. I_K1 channels are less promiscuous pharmacologically but are essential for cardiac excitability and arrhythmia susceptibility[7][9]. **Note:** The entry "hERG and I_K1" is not a canonical single target but rather combines two distinct cardiac potassium channels/currents, each encoded by separate genes and with separate roles, disease associations, and drug interaction profiles[7][9]. Each should be catalogued individually for structured pharmacological or biomedical purposes.

Other names

KCNH2Kv11.1Human ether-à-go-go-related geneEther-à-go-go potassium channelKir2.1KCNJ2Inward rectifier potassium channelI(K1)

hERG: Most drug interactions cause channel blockade, leading to prolongation of the cardiac QT interval (acquired long QT syndrome). I_K1: Blockers generally reduce inward rectifier current, destabilizing resting membrane potential.