Susan F. Steinberg, MD

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Overview
Credentials & Experience
Research

Overview

Academic Appointments

Professor of Molecular Pharmacology and Therapeutics

Credentials & Experience

Education & Training

BS, 1972 Biology, Massachusetts Institute of Technology
MD, 1976 Medicine, Harvard Medical School
Internship: 1977 Columbia Presbyterian Medical Center, NY
Residency: 1979 Columbia Presbyterian Medical Center, NY
Fellowship: 1982 Columbia Presbyterian Medical Center, NY

Honors & Awards

Thomas Smith Memorial Lecture, American Heart Associattion, 2019

Research

The studies in my laboratory aim to identify the mechanisms that underlie the physiologically important changes in cardiomyocyte adrenergic receptor responsiveness that accompany normal cardiac development, that influence the evolution of heart failure, or that contribute to cardiac injury in the setting of ischemia-reperfusion injury and oxidative stress. Our studies take advantage of a wide range of reductionist molecular and cell biological approaches in both cell culture and in vitro models to study the expression and subcellular localization of adrenergic receptor subtypes, to identify the adrenergic receptor binding partners and effectors that dictate signaling specificity in cardiomyocytes, and to understand the molecular basis for catecholamine-dependent cardiomyocyte remodeling. One area of particular interest has been the stimulus- (in some cases redox-) dependent post-translational modifications on signaling kinases such as protein kinase C and protein kinase D that alter their enzymology. We also have identified post-translational processing (involving an O-glycan-regulated proteolytic cleavage) of the beta1-adrenergic receptor N-terminus as a mechanism that calibrates signaling output to downstream effector responses. In both cases, these studies identify novel molecular determinants that can serve as druggable targets.

Selected Publications

Steinberg SF. N-tertaining a new signaling paradigm for the cardiomyocyte β1-adrenergic recepetor. J Cardiovasc Pharmacology (in press) 2022.
Zhu J and Steinberg SF. Trypsin cleavage of the β1-adrenergic receptor. Am J Physiol 322:H486-491, 2022
Zhu J and Steinberg SF. β1-adrenergic receptor N-terminal cleavage by ADAM17; the mechanism for redox-dependent downregulation of cardiomyocyte β 1-adrenergic receptors. J Mol Cell Cardiol 154:70-79, 2021.
Steinberg SF. Decoding the cardiac actions of protein kinase D isoforms. Mol Pharm 100:558-567, 2021
Alter S, Zimmer Ad, Park M, Gong J, Caliebe A, F?lster-Holst R, Torrelo A, Colmenero I, Steinberg SF, Fischer J. Telangiectasia - Ectodermal Dysplasia-Brachydactyly-Cardiac Anomaly-Syndrome is caused by de novo mutations in Protein Kinase D1. Human Genetics 58:415-421, 2021.
Park M and Steinberg SF. Carvedilol prevents redox inactivation of cardiomyocyte β1-adrenergic receptors. JACC: Basic to Translational Science 3:521-532, 2018.
Steinberg SF. Beta1-adrenergic receptor regulation revisited: the role of the extracellular N-terminus. Circ Res Viewpoint 123:1199-1201, 2018.
Steinberg SF. Post-translational modifications at the ATP-positioning G-loop that regulate protein kinase activity. Pharmacologic Research 135:181-187, 2018.
Park M, Reddy GR, Wallukat G, Xiang YK, and Steinberg SF. β1-adrenergic receptor O-glycosylation regulates N-terminal cleavage and signaling responses in cardiomyocytes. Scientific reports 7:7890, 2017.
Gong J and Steinberg SF. Cleavage alters the molecular determinants of protein kinase Cδ catalytic activity. Mol Cell Biol 37:e00324-17, 2017, 2017.
Qi W and Steinberg SF. Phos-tag SDS-PAGE resolves agonist- and isoform-specific activation patterns for PKD2 and PKD3 in cardiomyocytes and cardiac fibroblasts. J Mol Cell Card 99:14-22, 2016.
Gong J, Yao Y, Zhang P, Udayasuryan B, Komissarova E, Zhang F, Chen J Sivaramakrishnan S Van Eyk JE and Steinberg SF. The C2 domain and altered ATP-binding loop phosphorylation at Ser357 mediate the redox-dependent increase in protein kinase C-delta activity. Mol Cell Biol 35:1727-1740, 2015.


For a complete list of publications, please visit PubMed.gov