Barbara E Ehrlich, PhD Professor of Pharmacology and of Cellular And Molecular Physiology Department, Yale University School of Medicine New Haven
CT Calcium signaling and chemotherapy: New players and the prevention of side effects
The Ehrlich lab is interested in how cells regulate the intracellular calcium concentration. Cells use changes in calcium as a trigger for many cellular events, including muscle contraction, hormone secretion, and cell growth. The change in calcium levels can be modulated by the cell to tailor its response to the prevailing conditions. We have focused on one aspect of this process, the release of calcium from intracellular stores. We use biophysical, molecular and biochemical techniques to study the classes of calcium release channels known to exist inside virtually all cells the InsP3-gated channel, the ryanodine receptor/channel, and polycystin-2. The goal of the Ehrlich lab is to understand how the functions of these channels are altered by processes within the cell. The knowledge of how these channels work will form the background for studies of disease-induced changes in calcium release channel function. H.
Llewelyn Roderick, PhD Laboratory of Experimental Cardiology, Dept. of Cardiovascular Sciences, KULeuven
InsP¬3-mediated Ca2+ signalling during cardiac hypertrophy and failure
Work in the Roderick lab is focussed on understanding the role of InsP3 receptor channels and their activation downstream of Gq coupled receptors in cardiac function. In this regard, we aim to shed light upon how this channel that is expressed at a relatively low level and which influences global cytosolic calcium levels to a minimal extent, can exert its action in the cardiac myocyte. Our work has made important contributions to the notion that InsP3 signalling in functionally important cellular microdomains (the dyad and nucleus) allows calcium release via InsP3Rs to selectively influence excitation contraction coupling and hypertrophic gene expression. The amplification of InsP3R expression in disease adds to this capacity of InsP3Rs to affect cardiac function.