| Associate Professor 108 N. Greene St. Baltimore, MD 21201 Phone: 410-706-1615 Fax: 410-706-8297 email: kxu002@umaryland.edu
EDUCATION 1985 M.S., Department of Chemistry, University of California, San Diego, Chemistry 1988 Ph.D., Department of Chemistry, University of California, San Diego, Biochemistry POST GRADUATE EDUCATION Postdoctoral: 1988-1990 Harvard University School of Medicine and Massachusetts General Hospital, Biomedical Sciences. 1990-1992 Yale University School of Medicine, Molecular Biology
Instructor: 1992-1995 Johns Hopkins University School of Medicine, Department of Medicine, Division of Cardiology, Biomedical Sciences | |
PROFESSIONAL EXPERIENCE 1983-1988 Teaching Assistant, University of California San Diego 1988-1990 Postdoctoral Researcher, Harvard University School of Medicine 1990-1992 Postdoctoral Associate, Yale University School of Medicine 1992-1995 Instructor, Johns Hopkins University School of Medicine 1995–2003 Assistant Professor, Johns Hopkins University School of Medicine, Cardiology 2003–present Associate Professor, University of Maryland School of Medicine
RESEARCH DESCRIPTION Enzymes catalyze essential chemical reactions needed for living processes. (Na++K+)-ATPase (NKA) is one of the key enzymes that controls intracellular ion homeostasis and regulates cardiac function. For half a century, scientists have only known that inhibition of NKA induces a positive inotropic effect. Recently, we have discovered that activation of NKA markedly augments intracellular Ca2+ transient and cardiac contraction. The finding changes our traditional thinking about NKA and opens a new chapter of investigation. The current research concentrates on the molecular pathways, mechanisms, and regulations of activation of NKA medicated biological processes. We attempt to reveal the atomic basis of activation of NKA and to characterize the functional links between activation of NKA and the positive inotropy induced by it to advance our understanding of NKA in health and disease. Congestive heart failure is a major cause of death both in the United States and abroad. Understanding of the molecular regulation of NKA in cardiac function will help to develop new therapies to benefit heart failure patients.
SELECTED PUBLICATIONS Xu KY, Takimoto E, Juang GJ, Zhang Q, Rohde H, Myers AC. Evidence that the H1-H2 Domain of α1 Subunit of (Na++K+)-ATPase Participates in the Regulation of Cardiac Contraction, FASEB J (2005)19:53-61. Xu KY, Kuppusamy P. Dual Effects of Copper-Zinc Superoxide Dismutase. Biochem. Biophys. Res. Commun. (2005) 336:1190-1193 Xu KY. Activation of (Na++K+)-ATPase J. Gen. Physiol. (2005) 126:78-79. Xu KY. Activation of Na,K-ATPase Biochem. Biophys. Res. Commun. (2005)338:1669-1677 Xu KY, Kuppusamy SP, Wang JQ, Li H, Cui, H, Dawson TM, Huang PL, Burnett AL, Kuppusamy P, Becker, LC. Nitric Oxide Protects Cardiac Sarcolemmal Membrane Enzyme Function and Ion Active Transport Against Ischemia Induced Inactivation. J. Biol. Chem. (2003)278: 41798-41803. Xu KY, Huso DL, Dawson TM, Bredt DS, Becker LC. Nitric Oxide Synthase in Cardiac Sarcoplasmic Reticulum. Proc. Natl. Acad. Sci. (1999)96:657-662. Xu KY, Zweier JL, Becker LC. Hydroxyl Radical Inhibits Sarcoplasmic Reticulum Ca-ATPase Function by Direct Attack on the ATP Binding Site. Circ. Res. (1997)80:76-81. Xu KY, Zweier JL, Becker LC. Functional Coupling Between Glycolysis and Sarcoplasmic Reticulum Ca2+ Transport. Circ. Res. (1995)77:88-97. |