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Circulation Research|August 29, 1998
Modulation of cardiac Na+ current phenotype by beta1-subunit expressionS Kupershmidt, T Yang, D M RodenCirculation Research|December 1, 1995
Anti-minK antisense decreases the amplitude of the rapidly activating cardiac delayed rectifier K+ currentT Yang, S Kupershmidt, D M RodenCardiovascular Research|October 26, 1999
From genes to channels: normal mechanismsD M Roden, S KupershmidtThe Journal of Biological Chemistry|October 9, 1998
A K+ channel splice variant common in human heart lacks a C-terminal domain required for expression of rapidly activating delayed rectifier currentS Kupershmidt, D J Snyders, A Raes, et al.Circulation Research|February 5, 1999
Replacement by homologous recombination of the minK gene with lacZ reveals restriction of minK expression to the mouse cardiac conduction systemS Kupershmidt, T Yang, M E Anderson, et al.Circulation|February 1, 1996
Extracellular potassium modulation of drug block of IKr. Implications for torsade de pointes and reverse use-dependenceT Yang, D M RodenThe American Journal of Physiology|August 1, 1996
Regulation of sodium current development in cultured atrial tumor myocytes (AT-1 cells)T Yang, D M RodenJournal of Cardiovascular Pharmacology|October 17, 2001
Drug block of I(kr): model systems and relevance to human arrhythmiasT Yang, D Snyders, D M RodenCirculation Research|June 1, 1997
Rapid inactivation determines the rectification and [K+]o dependence of the rapid component of the delayed rectifier K+ current in cardiac cellsT Yang, D J Snyders, D M RodenCirculation|March 15, 1995
Ibutilide, a methanesulfonanilide antiarrhythmic, is a potent blocker of the rapidly activating delayed rectifier K+ current (IKr) in AT-1 cells. Concentration-, time-, voltage-, and use-dependent effectsT Yang, D J Snyders, D M RodenPageof 244