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Circulation Research|June 27, 2009
Protein kinase C{alpha}, but not PKC{beta} or PKC{gamma}, regulates contractility and heart failure susceptibility: implications for ruboxistaurin as a novel therapeutic approachQinghang Liu, Xiongwen Chen, Scott M Macdonnell, et al.
The Journal of Clinical Investigation|November 19, 2009
alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in miceHiroyuki Nakayama, Ilona Bodi, Robert N Correll, et al.
Circulation Research|April 2, 2016
Is Growth Differentiation Factor 11 a Realistic Therapeutic for Aging-Dependent Muscle Defects?Shavonn C Harper, Andrew Brack, Scott MacDonnell, et al.
Channels (Austin, Tex.)|July 21, 2020
A low voltage activated Ca2+ current found in a subset of human ventricular myocytesXin Zhang, Yijia Li, Xiaoying Zhang, et al.
Science Translational Medicine|January 10, 2020
HDAC inhibition improves cardiopulmonary function in a feline model of diastolic dysfunctionMarkus Wallner, Deborah M Eaton, Remus M Berretta, et al.
Journal of Molecular and Cellular Cardiology|May 22, 2012
Beta1-adrenergic receptors promote focal adhesion signaling downregulation and myocyte apoptosis in acute volume overloadRachid Seqqat, Xinji Guo, Khadija Rafiq, et al.
Circulation Research|February 12, 2005
Alterations in early action potential repolarization causes localized failure of sarcoplasmic reticulum Ca2+ releaseDavid M Harris, Geoffrey D Mills, Xiongwen Chen, et al.
Circulation Research|June 14, 2023
Functional LTCC-β2AR Complex Needs Caveolin-3 and Is Disrupted in Heart FailureJose L Sanchez-Alonso, Laura Fedele, Jaël S Copier, et al.
Circulation Research|September 19, 2013
Rejuvenation of human cardiac progenitor cells with Pim-1 kinaseSadia Mohsin, Mohsin Khan, Jonathan Nguyen, et al.
Journal of Cardiac Failure|June 11, 2005
The Na+/Ca2+ exchanger/SR Ca2+ ATPase transport capacity regulates the contractility of normal and hypertrophied feline ventricular myocytesJutta Weisser-Thomas, Hajime Kubo, Colleen A Hefner, et al.
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