Inward Rectifier Potassium Channels (Kir2.x) and Caveolin-3 Domain-Specific Interaction: Implications for Purkinje Cell-Dependent Ventricular Arrhythmias [Original Articles]

Conclusions Kir2.x isoforms have a unique intracellular pattern of distribution in association with specific Cav3 domains and that critically depends on interaction with N-terminal Kir2.x Cav3-binding motifs. Long-QT syndrome-9-CAV3 mutation differentially regulates current density and cell surface expression of Kir2.x homomeric and heteromeric channels. Mathematical Purkinje cell model incorporating experimental findings suggests delayed after-depolarization–type triggered activity as a possible arrhythmia mechanism.

http://circep.ahajournals.org/cgi/content/short/11/1/e005800?rss=1

Source: Circulation: Arrhythmia and Electrophysiology - January 11, 2018 Category: Cardiology Authors: Vaidyanathan, R., Van Ert, H., Haq, K. T., Morotti, S., Esch, S., McCune, E. C., Grandi, E., Eckhardt, L. L. Tags: Arrhythmias, Electrophysiology, Basic Science Research, Ion Channels/Membrane Transport, Translational Studies Original Articles Source Type: research