UMB School of Medicine

UMB School of Medicine Biochemistry & Molecular Biology

Kai Xu, Ph.D.
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.