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Potassium voltage-gated channel subfamily E member 1 (KCNE1) is a single-span transmembrane β-subunit that modulates the function of the KCNQ1 (Kv7.1) voltage-gated potassium channel. In the cardiac tissue, KCNE1 associates with KCNQ1 to form the IKs channel complex, which generates the slow delayed rectifier potassium current essential for the repolarization phase of the cardiac action potential. Mutations in KCNE1 or its alpha subunit partner KCNQ1 can result in cardiac arrhythmias, notably long QT syndrome and Jervell and Lange-Nielsen syndrome, sometimes accompanied by sensorineural deafness due to impaired potassium homeostasis. KCNE1 slows the channel's activation and changes conductance properties, thus regulating electrical signaling in excitable cells and affecting heart rate, neuronal excitability, and epithelial electrolyte transport. Drugs such as chromanol 293B and benzodiazepine L7 interact with the IKs complex, and KCNE1 is an important therapeutic and pharmacological target for managing QT interval abnormalities. Safety concerns center on arrhythmogenic risks and the potential for sudden cardiac death if the channel is abnormally modulated.
Blockade or inhibition of IKs current (by chromanol 293B, benzodiazepine L7). Modulation of channel gating kinetics and amplitude through β-subunit regulation.
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