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Ca2+/calmodulin-dependent kinase II-dependent signaling in disease

Among the longest standing efforts of our group has been to understand the relationship between CaMKII dysregulation and cardiac disease. Specifically, we have developed and applied novel experimental and computational tools to determine the underlying molecular mechanism for CaMKII-dependent regulation of voltage-gated Na+ channel activity, cell membrane excitability, and heart function.

Representative publications

Glynn P, Musa H, Wu X, Unudurthi SD, Little S, Qian L, Wright PJ, Radwanski PB, Gyorke S, Mohler PJ, Hund TJ. Voltage-gated sodium channel phosphorylation at Ser571 regulates late current, arrhythmias, and cardiac function in vivo. Circulation. 2015; 132:567-577. PMCID: PMC4543581.

Koval OM, Snyder JS, Wolf RM, Pavlovicz RE, Glynn P, Curran J, Leymaster ND, Dun W, Wright PJ, Cardona N, Qian L, Mitchell CC, Boyden PA, Binkley PF, Li C, Anderson ME, Mohler PJ, and Hund TJ. Ca2+/calmodulin-dependent protein kinase II-based regulation of voltage-gated Na+ channel in cardiac disease. Circulation. 2012; 126:2084-2094. PMCID: PMC3811023.

Christensen MD, Dun W, Boyden PA, Anderson ME, Mohler PJ, and Hund TJ. Oxidized calmodulin kinase II regulates conduction following myocardial infarction: A computational analysis. PLoS Comput Biol. 2009; 5:e1000583. PMCID: PMC2778128.

Hund TJ, Decker KF, Kanter E, Mohler PJ, Boyden PA, Schuessler RB, Yamada KA, Y Rudy. Role of activated CaMKII in abnormal calcium homeostasis and INa remodeling after myocardial infarction: Insights from mathematical modeling. J Mol Cell Cardiol. 2008;45:420-8. PMCID: PMC2587155.