Potassium voltage-gated channel subfamily E regulatory subunit 1 (KCNE1) (KCNE1)

Potassium voltage-gated channel subfamily E regulatory subunit 1 (KCNE1), historically referred to as hIsK or MinK, is a single-transmembrane protein that acts as a vital ancillary subunit for the KCNQ1 (Kv7.1) potassium channel (UniProt: P15382). This protein does not form a functional channel on its own but dramatically alters the gating kinetics and conductance of KCNQ1 to produce the slowly activating delayed rectifier potassium current (IKs) in cardiac myocytes (PubMed: 10371522). This current is essential for terminating the cardiac action potential and maintaining the repolarization reserve, particularly during periods of high heart rate or sympathetic activation. Mutations in KCNE1 are clinically significant, leading to Long QT Syndrome type 5 (LQT5) and, when biallelic, Jervell and Lange-Nielsen Syndrome, which is characterized by both cardiac arrhythmias and profound deafness (NCBI Gene: 3753). Because of its central role in cardiac electrophysiology, the KCNQ1-KCNE1 complex is a major focus for anti-arrhythmic drug development and a key site for potential drug-induced cardiotoxicity (PubMed: 25135974). Selective modulation of this target offers a pathway for treating rhythm disorders, though it requires precise control to avoid excessive prolongation of the QT interval and subsequent risk of Torsades de Pointes (StatPearls: Long QT Syndrome).

Other names

MinKIsKMinimal potassium channel proteinIKs producing subunithIsK

Modulation of the KCNQ1-KCNE1 channel complex to inhibit or enhance the slowly activating delayed rectifier potassium current (IKs).