Article
Insulin suppresses IKs (KCNQ1/KCNE1) currents, which require β-subunit KCNE1.
Pflugers Archiv : European journal of physiology - 1 May 2014
Wu Minghua, Obara Yutaro, Norota Ikuo, Nagasawa Yoshinobu, Ishii Kuniaki
Abstract excerpt
Abnormal QT prolongation in diabetic patients has become a clinical problem because it increases the risk of lethal ventricular arrhythmia. In an animal model of type 1 diabetes mellitus, several ion currents, including the slowly activating delayed rectifier potassium current (IKs), are altered. The IKs channel is composed of KCNQ1 and KCNE1 subunits, whose genetic mutations are well known to cause long QT...
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