Abstract
Slow deactivation is a critical biophysical and physiological property of human ether-à-go-go-related gene (hERG) channels mediating the cardiac repolarizing current IKr. Disruption of direct interactions between the intracellular N-terminal eag domain and the C-terminal cyclic nucleotide binding homology domain (CNBhD) can impair slow repolarization and are associated with disease. The eag domain is multipartite: it comprises an N-terminal Per-Arnt-Sim (PAS) cap (residues 1-25) and globular PAS domain (residues 26-135).
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