IKs, a Slow and Intriguing Cardiac K+ Channel and Its Associated Long QT Diseases
Author:
Publisher
Elsevier BV
Subject
Cardiology and Cardiovascular Medicine
Reference65 articles.
1. The sympathic imbalance hypothesis of QT interval prolongation;Abildskov;J Cardiovasc Electrophysiol,1991
2. Characterization of two distinct depolarization-activated K+ currents in isolated adult rat ventricular myocytes;Apkon;J Gen Physiol,1991
3. The protein IsK is a dual activator of K+ and Cl− channels;Attali;Nature,1993
4. A corticosteroid-induced gene ex-pressing an “IsK-like” K+ channel activity in Xenopus oocytes;Attali;Proc Natl Acad Sci USA,1995
5. K(v)LQT1 and IsK (minK) proteins associate to form the I-Ks cardiac potassium current;Barhanin;Nature,1996
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1. β-adrenergic stimulation augments transmural dispersion of repolarization via modulation of delayed rectifier currents IKs and IKr in the human ventricle;Scientific Reports;2017-11-21
2. Comparison of electrophysiological effects of calcium channel blockers on cardiac repolarization;The Korean Journal of Physiology & Pharmacology;2016
3. Role of slow delayed rectifying potassium current in dynamics of repolarization and electrical memory in swine ventricles;The Journal of Physiological Sciences;2014-03-30
4. Characterization of binding site of closed-state KCNQ1 potassium channel by homology modeling, molecular docking, and pharmacophore identification;Biochemical and Biophysical Research Communications;2005-07
5. Cardiac-enriched LIM domain protein fhl2 is required to generate IKs in a heterologous system;Cardiovascular Research;2002-10
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