Imbalances in membrane excitability underlie a broad range of cardiac arrhythmias and conduction defects. Although we now know the genes encoding almost all ion channels, we have little understanding of how the macromolecular composition and relative numbers of different channel types is achieved to exert exquisite control over membrane potential changes in time. Even minor changes in this balance can lead to sudden cardiac death and disturbances of membrane excitability in many other systems.
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