Our research team focuses on the cellular mechanisms underlying the genesis and control of cardiac automaticity. In the past, we have introduced the use of genetically-modified mice in the study of pacemaker activity and described the role of L-type Cav1.3 and T-type Cav3.1 calcium channels in cardiac automaticity and coduction in mice and humans. Our group now studies the complex interactions between ion channels of the plasma membrane and intracellular pathways underlying pacemaking, as well as their impact in diseases of cardiac automaticity.
