KCNQ1 and minK form the slow delayed rectifier potassium current, IKs in the heart. This multimeric ion channel contributes to cardiac action potential repolarization and determines the heartbeat rate. Mutations in either KCNQ1 or minK that reduce IKs have been shown to cause long-QT syndrome (LQTS), a disorder of ventricular repolarization that can result in cardiac arrhythmia and sudden death. A well-recognized potential treatment for LQTS caused by reduction of IKs is to enhance functional activation of cardiac KCNQ1/minK channels.

Product Information
Catalog #:	ACC-RI0023
Gene Name	KCNQ1/MINK1
Abbr	CHO-HuKCNQ1/MINK1
Alias	MINK1,hMINK,hMINKbeta,MGC21111,
Growth Properties	Adherent
Host Cell	CHO-K1
Morphology	Epithelial-like
Shipping	Dry ice
Product Type	Ion Channel Expressing Cell
Channel Type	Potassium Channel
Channel Subgroup	Kv7.1
Species	Human
Product Format	frozen
searchKeyword	MINK1,hMINK,hMINKbeta,MGC21111,