Nav1.5 N-terminal domain binding to {alpha}1-syntrophin increases membrane density of human Kir2.1, Kir2.2 and Nav1.5 channels

Conclusions
The results demonstrate the critical role of the N-terminal domain of Nav1.5 channels in Nav1.5–Kir2.x-reciprocal interactions and suggest that the molecular mechanisms controlling atrial and ventricular cellular excitability may be different.

Source: Cardiovascular Research - April 18, 2016 Category: Cardiology Authors: Matamoros, M., Perez-Hernandez, M., Guerrero-Serna, G., Amoros, I., Barana, A., Nunez, M., Ponce-Balbuena, D., Sacristan, S., Gomez, R., Tamargo, J., Caballero, R., Jalife, J., Delpon, E. Tags: Ion Channels and Arrhythmias Source Type: research