The laboratory is focused on investigating the molecular mechanism governing contractility in smooth (Fig 1) and cardiac muscle, and uses technically demanding, state-of-the-art mechanical, molecular, biochemical and transgenic techniques (Fig 2).
Currently there are three major research projects in the laboratory. One project focuses on the molecular determinants, or protein structure (Fig 3), for the kinetics of the actomyosin ATPase (Fig 4) and force maintenance in smooth muscle. We have recently begun investigating the role of nonmuscle myosin II in defining the tonic contractile phenotype as well as its participation in smooth muscle contraction. Another project is designed to investigate the mechanism and signaling pathway used for nitric oxide mediated vasodilatation (Fig 5). The final project is to determine the mechanism for the decrease in sensitivity to nitric oxide in patients with heart failure. In addition, we have begun a project to investigate the mechanism of the defect in cardiac contractility that occurs with a prolonged decrease in blood flow; or the mechanism for myocardial hibernation.
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