Slow delayed rectifier potassium channel (IKs)

The slow delayed rectifier potassium channel, commonly known as IKs, is a voltage-gated ion channel primarily located in the heart and inner ear (UniProt: P51787). It is formed by the co-assembly of the KCNQ1 alpha-subunit and the KCNE1 beta-subunit, which significantly slows the activation kinetics and increases the current density compared to KCNQ1 alone (PubMed: 8599120). In the heart, IKs plays a critical role in the late phase of repolarization of the cardiac action potential, especially during sympathetic stimulation or increased heart rates (StatPearls: NBK538143). Mutations in the genes encoding this channel are a leading cause of hereditary Long QT syndrome (LQT1) and Jervell and Lange-Nielsen syndrome, which predispose individuals to life-threatening arrhythmias (PubMed: 11854046). Pharmacological modulation of IKs is a target for anti-arrhythmic therapy, though inhibitors carry the risk of inducing QT prolongation and sudden cardiac death (PubMed: 15131015). Conversely, activators are being explored as potential treatments for shortening the QT interval in patients with certain forms of congenital Long QT syndrome (PubChem: CID 10429204).

Other names

IKs channelKCNQ1/KCNE1 complexKv7.1/MinK complexSlowly activating delayed rectifier potassium channel

Modulation of the channel's gating kinetics or pore conductance to either shorten or prolong the cardiac action potential duration (PubMed: 11854046).