Multiplex kinase signaling modifies cardiac function at the level of sarcomeric proteins

[1] α1-AR-induced positive inotropic response in heart is dependent on myosin light chain phosphorylation [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2002, 283 (04): : H1471 - H1480

[2] β3-Adrenoceptors modulate left ventricular relaxation in the rat heart via the NO-cGMP-PKG pathway [J]. ACTA PHYSIOLOGICA, 2008, 193 (03) : 229 - 239

[3] Protein kinase D in the cardiovascular system - Emerging roles in health and disease [J]. CIRCULATION RESEARCH, 2008, 102 (02) : 157 - 163

[4] Augmented protein kinase C-α-induced myofilament protein phosphorylation contributes to myofilament dysfunction in experimental congestive heart failure [J]. CIRCULATION RESEARCH, 2007, 101 (02) : 195 - 204

[5] Bers D.M., 2001, Excitation-Contraction Coupling and Cardiac Contractile Force, V2th

[6] Increased protein kinase C activity and expression of Ca2+-sensitive isoforms in the failing human heart [J]. CIRCULATION, 1999, 99 (03) : 384 - 391

[7] Phosphorylation or glutamic acid substitution at protein kinase C sites on cardiac troponin I differentially depress myofilament tension and shortening velocity [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (13) : 11265 - 11272

[8] Length and protein kinase A modulations of myocytes in cardiac myosin binding protein C-deficient mice [J]. CARDIOVASCULAR RESEARCH, 2006, 69 (02) : 370 - 380

[9] Opposing cardioprotective actions and parallel hypertrophic effects of δPKC and εPKC [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (20) : 11114 - 11119

[10] Myosin-binding protein C phosphorylation, myofibril structure, and contractile function during low-flow ischemia [J]. CIRCULATION, 2005, 111 (07) : 906 - 912

[1] α1-AR-induced positive inotropic response in heart is dependent on myosin light chain phosphorylation [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2002, 283 (04): : H1471 - H1480

[2] β3-Adrenoceptors modulate left ventricular relaxation in the rat heart via the NO-cGMP-PKG pathway [J]. ACTA PHYSIOLOGICA, 2008, 193 (03) : 229 - 239

[3] Protein kinase D in the cardiovascular system - Emerging roles in health and disease [J]. CIRCULATION RESEARCH, 2008, 102 (02) : 157 - 163

[4] Augmented protein kinase C-α-induced myofilament protein phosphorylation contributes to myofilament dysfunction in experimental congestive heart failure [J]. CIRCULATION RESEARCH, 2007, 101 (02) : 195 - 204

[5] Bers D.M., 2001, Excitation-Contraction Coupling and Cardiac Contractile Force, V2th

[6] Increased protein kinase C activity and expression of Ca2+-sensitive isoforms in the failing human heart [J]. CIRCULATION, 1999, 99 (03) : 384 - 391

[7] Phosphorylation or glutamic acid substitution at protein kinase C sites on cardiac troponin I differentially depress myofilament tension and shortening velocity [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (13) : 11265 - 11272

[8] Length and protein kinase A modulations of myocytes in cardiac myosin binding protein C-deficient mice [J]. CARDIOVASCULAR RESEARCH, 2006, 69 (02) : 370 - 380

[9] Opposing cardioprotective actions and parallel hypertrophic effects of δPKC and εPKC [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (20) : 11114 - 11119

[10] Myosin-binding protein C phosphorylation, myofibril structure, and contractile function during low-flow ischemia [J]. CIRCULATION, 2005, 111 (07) : 906 - 912