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Research Description:
Dr. Jiang’s laboratory is interested how environmental conditions, such as nutrient and stresses, control cell growth and proliferation. The laboratory focuses on intercellular signal transduction pathways that sense and transmit the environmental cues to cellular machinery governing metabolism and biosynthesis. Understanding how these pathways work in normal and cancer cells would allow us to development drugs for cancer prevention. Dr. Jiang’s laboratory studies the mechanism underlying the action of rapamycin, a macrolide antibiotic that has been used clinically as immunosuppressant for transplantation and anti-neoplastic drug for cancer prevention. The intracellular target of rapamycin is a kinase called TOR (or mTOR in mammalian cells), which lies at the center of a signaling network that controls many growth-related cellular events in response to changes in nutrient, growth factor, oxygen and energy levels. His laboratory is currently trying to answer two key questions concerning the signaling mechanisms of TOR: 1) how is TOR regulated by many distinct upstream signals? 2) what are the mechanisms by which TOR control many diverse cellular events. Several projects centering on these two questions are ongoing.  The first project concerns the mechanism that controls mTOR. Jiang’s laboratory has recently identified FKBP38, a member of the FK506 binding protein family, as an endogenous inhibitor of mTOR. They are trying to determine how nutrient, growth factor and oxygen levels regulate mTOR through FKBP38 in mammalian systems. The second project aims to the role of FKBP38 in apoptosis. FKBP38 has been shown to interact with the anti-apoptotic proteins, Bcl-2 and Bcl-xL. Jiang’s laboratory is investigating whether nutrient, growth factor and oxygen levels control the anti-apoptotic activity of Bcl-2 and Bcl-xL through FKBP38 in mammalian systems. The third project focuses on the mechanism by which TOR elicits its pleiotropic roles in cell growth. Recent studies in Jiang’s laboratory have established protein phosphatase 2A as a major downstream target of the Tor pathway. His laboratory is currently investigating how Tor mediates PP2A activity and how PP2A relays Tor signaling activity to many cellular processes using yeast Saccharomyces cerevisiae as a model system.
Education:
B.A. (Genetics), Sichuan University, Sichuan, China, 1985.
M.S. (Molecular Biology), Graduate School of the University of Science and Technology of China, Beijing, China, 1988.
Ph.D. (Cell Biology), Yale University, 1995.
Postdoctoral Fellow, Princeton University, 2000.
Important Publications:
- Ma D, X Bai, H Gou and Y Jiang. Rheb GTPase controls apoptosis by regulating interaction of FKBP38 with Bcl-2 and Bcl-XL. J Biol Chem 285:8621-8627, 2010
- Bommareddy A, ER Hahm, D Xiao, AA Powolny, A Fisher, Y Jiang and SV Singh. ATG5 regulates phenethyl isothiocyanate-induced autophagic and apoptotic cell death in human prostate cancer cells. Cancer Research 69:3704-3712, 2009
- Guo S, X Shen, G Yan, D Ma, X Bai, S Li and Y Jiang. A MAP kinase dependent feedback mechanism controls Rho1 GTPase and actin distribution in yeast. PLos One 4:e6089, 2009
- Ma D, X Bai, S Guo and Y Jiang. The switch I region of Rheb is critical for its interaction with FKBP38. J Biol Chem 283:25963-25970, 2008
- Bai X, D Ma, A Liu, X Shen, QJ Wang, Y Liu and Y Jiang. Rheb activates mTOR by antagonizing its endogenous inhibitor, FKBP38. Science 318:977-980, 2007
- Jiang Y. Regulation of the cell cycle by protein phosphatase 2A in yeast. Microbio Mol Biol Review 70(2):440-449, 2006
- Yan C, X Shen and Y Jiang. Rapamycin activates the Tap42-associated phosphatases by abrogating their association with Tor complex 1. EMBO J 25(15):3546-3555, 2006
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