Article
Arrhythmogenic calmodulin mutations disrupt intracellular cardiomyocyte Ca2+ regulation by distinct mechanisms.
Journal of the American Heart Association - 23 Jun 2014
Yin Guo, Hassan Faisal, Haroun Ayman R, Murphy Lisa L, Crotti Lia, Schwartz Peter J, George Alfred L, Satin Jonathan
Abstract excerpt
BACKGROUND: Calmodulin (CaM) mutations have been identified recently in subjects with congenital long QT syndrome (LQTS) or catecholaminergic polymorphic ventricular tachycardia (CPVT), but the mechanisms responsible for these divergent arrhythmia-susceptibility syndromes in this context are unknown. We tested the hypothesis that LQTS-associated CaM mutants disrupt Ca2+ homeostasis in developing cardiomyocytes...
Topics
- Animals
- Arrhythmias, Cardiac
- Calcium
- Calcium Channels, L-Type
- Calmodulin
- Cells, Cultured
- Genetic Predisposition to Disease
- Homeostasis
- Humans
- Long QT Syndrome
- Mice, Inbred ICR
- Mutation
- Myocytes, Cardiac