Tung Chan, Ph.D.

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. Induced overexpression of Na+/Ca2+ exchanger transgene: Altered myocyte contractility, [Ca2+]i transients, SR Ca2+ contents, and action potential duration
2. TNF-α reduces PGC-1α expression through NF-κB and p38 MAPK leading to increased glucose oxidation in a human cardiac cell model
3. Akt is a direct target of the phosphatidylinositol 3-kinase: Activation by growth factors, v-src and v-Ha-ras, in Sf9 and mammalian cells
4. The Gfi-1 protooncoprotein represses Bax expression and inhibits T-cell death
5. Regulation of cardiac myocyte contractility by phospholemman: Na +/Ca2+ exchange versus Na+-K+-ATPase
6. A1 adenosine receptor upregulation accompanies decreasing myocardial adenosine levels in mice with left ventricular dysfunction
7. AKT and CDK5/p35 mediate brain-derived neurotrophic factor induction of DARPP-32 in medium size spiny neurons in vitro
8. Regulated overexpression of the A1-adenosine receptor in mice results in adverse but reversible changes in cardiac morphology and function
9. Cardioprotection afforded by NF-κB ablation is associated with activation of Akt in mice overexpressing TNF-α
10. Cooperative regulation of p70S6 kinase by receptor tyrosine kinases and G protein-coupled receptors augments airway smooth muscle growth
11. Tumor Necrosis Factor Receptors 1 and 2 Differentially Regulate Survival, Cardiac Dysfunction, and Remodeling in Transgenic Mice with Tumor Necrosis Factor-α-Induced Cardiomyopathy
12. The Balance Between Pro-Apoptotic and Anti-Apoptotic Pathways in the Failing Myocardium
13. Targeting the epidermal growth factor receptor in cancer: Apoptosis takes center stage
14. Small GTPases and tyrosine kinases coregulate a molecular switch in the phosphoinositide 3-kinase regulatory subunit
15. PDK2: a complex tail in one Akt.
16. Rit, a non-lipid-modified Ras-related protein, transforms NIH3T3 cells without activating the ERK, JNK, p38 MAPK or PI3K/Akt pathways
17. AKT/PKB and other D3 phosphoinositide-regulated kinases: Kinase activation by phosphoinositide-dependent phosphorylation
18. Differential roles of Akt, Rac, and Ral in R-Ras-mediated cellular transformation, adhesion, and survival
19. Akt activation by growth factors is a multiple-step process: The role of the PH domain
20. Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway

View All Publications