Ivy E. Dick

Biography

I began my studies of ion channels as an electrophysiologist at Merck in the laboratories of Dr. Charles Cohen and Dr. Owen McManus where I characterized the pharmacological modulation of voltage gated sodium channels. In 2004, I joined the Calcium Signals Lab at Johns Hopkins as a graduate student under the direction of Dr. David Yue. My research focused on understanding the spatial selectivity of calmodulin regulation of voltage gated calcium channels. Upon graduation, I elected to remain in the Calcium Signals lab for my post-doctoral research and later as a Research Associate, and continued my research on the mechanisms underlying calmodulin regulation of calcium channels, and how those mechanisms are disrupted in Timothy Syndrome.

Research Interest

Voltage-gated calcium channels (CaV) are critical conduits for Ca2+ entry into the heart, smooth muscle and brain. Ca2+ entry through these channels must be precisely controlled, thus these channels employ two major forms of feedback regulation: voltage dependent inactivation (VDI) and Ca2+ dependent inactivation (CDI). Disruption of these important regulatory processes results in severe clinical phenotypes including autism, ataxia and long QT syndrome. My research has focused on gaining mechanistic understanding of these regulatory processes, and applying those findings to gain new insight into the pathogenesis and treatment options for Ca2+ channelopathies and related diseases. Recent work has focused on unraveling the mechanisms leading to cardiac arrhythmias in calcium channelopathies such as Timothy Syndrome (TS). By examining the inactivation defects underlying two different L-type channel TS mutations, we uncovered a remarkable divergence in the mechanisms leading to deficits in CDI. These findings promise new insight into customized treatment for TS, and illustrate how in depth biophysical understanding can inform on therapeutic interventions in patients. Overall, my lab studies the mechanisms underlying the regulation of voltage-gated calcium channels, how these mechanisms are disrupted by genetic mutations, and how new therapeutic strategies can address these disruptions.