Potassium voltage-gated channel subfamily KQT member 1 and Potassium voltage-gated channel subfamily E member 1 (KCNQ1 (for Potassium voltage-gated channel subfamily KQT member 1) and KCNE1 (for Potassium voltage-gated channel subfamily E member 1). When referencing the functional cardiac complex, the common abbreviation is KCNQ1/KCNE1 or "IKs channel.")

The cardiac **IKs channel** is a protein complex composed of four **KCNQ1** (Potassium voltage-gated channel subfamily KQT member 1) subunits forming the pore and typically two **KCNE1** (Potassium voltage-gated channel subfamily E member 1) subunits acting as regulatory β-subunits[1][2][3]. This complex is a voltage-gated potassium channel critical for **electrical repolarization of cardiomyocytes** during the cardiac action potential and for maintaining ion homeostasis in epithelial tissues and the inner ear[1][2][3][4][5]. In the heart, KCNQ1/KCNE1 activity underlies the “slow delayed rectifier” potassium current (IKs), and mutations or pharmacological inhibition can lead to life-threatening arrhythmias such as long QT syndrome. In the inner ear, these channels maintain potassium balance required for normal hearing. The functional properties of the KCNQ1/KCNE1 complex are distinct from either protein alone; KCNE1 modulates KCNQ1 by slowing activation kinetics, enhancing conductance, and stabilizing the open state. Both genetic mutations and drug interactions with this channel complex are major causes of inherited and acquired arrhythmias[1][2][3][4][5].

Other names

KCNQ1: Kv7.1KVLQT1KCNE1: MinKIKs channel (for the KCNQ1/KCNE1 complex)

Inhibition of potassium efflux conducted by the KCNQ1/KCNE1 complex, prolonging cardiac action potential and refractory period (antiarrhythmic effect) - In some cases, activation of channel function (fewer examples, investigational)