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Molecular Screen Identifies Cardiac Myosin-Binding Protein-C as a Protein Kinase G-Iα Substrate.
Circ Heart Fail
November 2015
From the Molecular Cardiology Research Institute (R.T., G.-R.W., T.D.C., R.M.B.) and Division of Cardiology (R.M.B.), Tufts Medical Center, Boston, MA; Tufts University School of Medicine, Boston, MA (S. Giovanni); Department of Cell and Molecular Physiology, Health Sciences Division, Loyola University Chicago, Maywood, IL (S. Govindan, S.S.); Johns Hopkins Medical Institutions, Baltimore, MD (D.I.L., E.T., D.A.K.); and Department of Cardiovascular Medicine, The University of Tokyo, Tokyo, Japan (E.T.).
Background: Pharmacological activation of cGMP-dependent protein kinase G I (PKGI) has emerged as a therapeutic strategy for humans with heart failure. However, PKG-activating drugs have been limited by hypotension arising from PKG-induced vasodilation. PKGIα antiremodeling substrates specific to the myocardium might provide targets to circumvent this limitation, but currently remain poorly understood.
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