Tung Chan, PhD

Contact Dr. Chan

Center for
Translational Medicine
1025 Walnut Street, Suite 412
Philadelphia, PA 19107

(215) 955-4231
(215) 503-4741 fax

Degree
Ph.D. University of Calgary, Alberta, Canada 1993

University Appointment
Assistant Professor of Medicine, 2003-current

Research and Clinical Interests
Dr. Chan's laboratory is investigating the roles of PI3K/Akt survival signals and adenosine G-protein-coupled receptors in heart failure development. Current projects include:

(1) Using an inducible and heart-specific promoter to activate adenosine receptors in mouse heart;

(2) Studying the contribution of individual Akt subtypes in heart failure development with Akt subtype-specific knockout mice;

(3) Using embryonic stem cells to determine novel mechanisms of Akt regulation and cardiomyocyte differentiation.

Dr. Chan believes that his research will help to advance heart disease therapeutics and to minimize cardiotoxic side effects of anti-cancer therapeutics.

Publications

Most Recent Peer-reviewed Publications

1. Cardioprotection of controlled and cardiac-specific over-expression of a2A-adenosine receptor in the pressure overload
2. Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: Potential involvement of Na +/Ca 2+ exchanger
3. Autoregulation of kinase dephosphorylation by ATP binding to AGC protein kinases
4. Resistance of Akt kinases to dephosphorylation through ATP-dependent conformational plasticity
5. Myocardial injury after ischemia-reperfusion in mice deficient in Akt2 is associated with increased cardiac macrophage density
6. Adenosine receptor subtypes and the heart failure phenotype: translating lessons from mice to man.
7. Residues 248-252 and 300-304 of the cardiac naspi +/Ca 2+ exchanger are involved in its regulation by phospholemman
8. Controlled and cardiac-restricted overexpression of the arginine vasopressin V1A receptor causes reversible left ventricular dysfunction through Ga q-mediated cell signaling
9. The interplay between NF-kappab and E2F1 coordinately regulates inflammation and metabolism in human cardiac cells
10. Regulation of in vivo cardiac contractility by phospholemman: Role of Na +/Ca 2+ exchange
11. Left ventricular dysfunction in murine models of heart failure and in failing human heart is associated with a selective decrease in the expression of caveolin-3
12. The p65 subunit of NF-B binds to PGC-1, linking inflammation and metabolic disturbances in cardiac cells
13. Phospholemman: A novel cardiac stress protein
14. Effects of cardiac-restricted overexpression of the A2A adenosine receptor on adriamycin-induced cardiotoxicity
15. Phospholemman and β-adrenergic stimulation in the heart
16. Induced overexpression of Na+/Ca2+ exchanger transgene: Altered myocyte contractility, [Ca2+]i transients, SR Ca2+ contents, and action potential duration
17. TNF-α reduces PGC-1α expression through NF-κB and p38 MAPK leading to increased glucose oxidation in a human cardiac cell model
18. Cardiac-restricted overexpression of the A2A-adenosine receptor in FVB mice transiently increases contractile performance and rescues the heart failure phenotype in mice overexpressing the A1-adenosine receptor
19. Regulation of cardiac myocyte contractility by phospholemman: Na +/Ca2+ exchange versus Na+-K+-ATPase
20. A1 adenosine receptor upregulation accompanies decreasing myocardial adenosine levels in mice with left ventricular dysfunction

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