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Thomas Jefferson University - Thomas L Force, M.D.
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Thomas L Force, M.D.
Cardiology
Thomas L. Force, M.D.
James C. Wilson Professor of Medicine
Clinical Director, Center for Translational Medicine
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Mailing Address
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1025 Walnut Street, 316 College Building
Philadelphia, Pennsylvania 19107
United States
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Expertise and Research Interests
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My lab focuses on the regulation of normal and stress-induced cardiomyocyte hypertrophy. Specifically, we study the signal transduction pathways that regulate growth responses, focusing on protein kinase cascades. Most recently, we have studied the role of glycogen synthase kinase-3beta, which is a potent negative regulator of growth, and its downstream targets, which include beta-catenin and its co-factors, the Tcf family of transcription factors, and the family of nuclear factors of activated T cells (NF-ATs), in hypertrophic growth. In addition, we study signaling mechanisms that regulate the response of the cell to ischemic injury. Making use of novel small molecule inhibitors, we have recently identifyied a novel mechanism by which the JNK family of stress-activated protein kinases regulate activity of the pro-survival kinase, Akt/PKB, and, via this mechanism, cardiomyocyte survival following ischemia/reperfusion.
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Publications
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- Pombo CM, Kehrl JH, Sanchez I, Katz P, Avruch J, Zon LI, Woodgett JR, Force T, Kyriakis JM: Activation of the SAPK pathway by the human STE20 homologue, germinal centre kinase. Nature: 377: 750-754, 1995
- Pombo C, Bonventre JV, Molnar A, Kyrakis J, Force T. Activation of a human Ste20-like kinase by oxidant stress defines a novel stress response pathway. EMBO J.:15: 4537-4546, 1996.
- Choukroun G, Hajjar R, Kyriakis JM, Bonventre JV, Rosenzweig A, Force T. Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy. J. Clin. Invest. 102: 1311-1320, 1998.
- Haq S, Choukroun G, Kang ZB, Lee K-H, Ranu H, Matsui T, Rosenzweig A, Alessandrini A, Molkentin JD, Woodgett J, Hajjar R, Michael A, Force T. Glycogen synthase kinase-3ß is a negative regulator of cardiomyocyte hypertrophy. J. Cell Biol. 151: 117-129, 2000.
- Sheridan AM, Force T, Yoon, H.J., Choukroun, G., OLeary E, Taheri, M.R. Bonventre JV: PLIP, a novel splice variant of TIP60, interacts with Group IV cPLA2, induces apoptosis and potentiates prostaglandin production. Mol. Cell. Biol. 14: 4470-4481, 2001.
- Haq S, Michael A, Andreucci M, Bhattacharya K, Dotto P, Walters BL, Woodgett J, Kilter H, Force T. Stabilization of ß-catenin by a Wnt-independent mechanism regulates cardiomyocyte growth. Proc Natl Acad Sci 100:4610-15, 2003.
- Haq S, Kilter H, Michael A, Tao J, OLeary E, Sun XM, Walters B, Bhattacharya K, Chen X, Cui L, Andreucci M, Rosenzweig A, Guerrero JL, Patten R, Liao R, Molkentin J, Picard M, Bonventre JV, Force T. Deletion of cytosolic phospholipase A2 promotes striated muscle growth. Nat Med: 9:944-951, 2003.
- Michael A, Haq S, Chen X, Hsich E, Cui L, Walters B, Shao Z, Bhattacharya K, Kilter H, Huggins G, Andreucci M, Periasamy M, Solomon RN, Liao R, Patten R, Molkentin JD, Force T. GSK-3b regulates growth, calcium homeostasis and diastolic function in the heart. J. Biol. Chem.. 279: 21383, 2004.
- Shao Z, Bhattacharya K, Hsich E, Park L, Walters B, Germann U, Wang Y-M, Kyriakis J, Mohanlal R, Kuida K, Namchuk M, Salituro F, Yao Y-M, Hou W-M, Chen X, Aronovitz M, Tsichlis PN, Bhattacharya S, Force T, Kilter H. c-Jun N-terminal kinases mediate reactivation of Akt and cardiomyocyte survival after hypoxic injury in vitro and in vivo. Circ. Res. 98: In press, 2006.
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Individual Expertise profile of
Thomas L Force, M.D., Copyright © Thomas L Force, M.D..
Last Updated
by Admin
: Friday, October 9, 2009 10:11:55 AM
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