We are interested in understanding the regulation of ion channels by diverse G-protein signaling pathways in normal and pathological states.
One major focus of our current work involves the changes in function and regulation of cardiac ion channels that lead to the pathogenesis of the Long QTsyndrome. Our work attempts to translate channel function and dysregulation at the cellular level to patient clinical phenotype and response to treatment.
A second focus of our current research is the study of the pathological remodeling of the slow delayed rectifier-like current (IKs) in heart failure. KCNQ1 is co-assembled with the KCNE1 gene product in the heart to produce IKs, which is one of the main currents responsible for myocyte repolarization. The most commonly inherited cardiac arrhythmia, long-QT1 (LQT1), is due to mutations in the KCNQ1 potassium channel. Heart disease is also known to decrease IKs currents. Our current research focus on stress signals caused by chronic stimulation of kinase signaling pathways, and their consequence for ion channel function and membrane trafficking. We explore possible novel antiarrhythmic treatments to reverse IKs pathological remodeling during heart failure.
