The Jiang lab is interested in the signaling mechanism by which Tor mediates cell growth and proliferation. Tor, a homologue of ATM and the DNA dependent kinase, is a key regulator of cell growth and proliferation in most eukaryotic cells. It is also the target of the immunosuppressive drug rapamycin, which exerts its anti-inflammatory effect by specifically inhibiting Tor function in lymphoid cells. Tor controls many diverse cellular processes in response to both nutrient and growth factor signals. Emerging evidence suggests that Tor acts as a checkpoint protein to impinge nutrient signals into growth factor mediated processes. In this view, Tor activity ensures that cell growth occurs only when the nutrient requirement is met. The lab has been using yeast Saccharomyces cerevisiae as a model system to study Tor mediated signaling pathway. Recent studies in his laboratory have established protein phosphatase 2A as a major downstream target of the Tor signaling. His laboratory is currently investigating how Tor mediates PP2A activity and how PP2A relays Tor signaling activity to many cellular processes.
Dr. Jiang’s laboratory is interested in intracellular signaling pathways governing cell growth and metabolism. The laboratory’s current research projects concern the signaling mechanism of the mammalian target of rapamycin (mTOR). mTOR is a protein ser/thr kinase that plays a key role in translation, autophagy and mitochondrial biogenesis. Its activity is regulated by signals of various origins, including nutrient, growth factor, energy and stress. The laboratory has previously identified FKBP38 that acts as an inhibitor of mTOR. Three projects centering on the role of FKBP38 in mTOR regulation are on-going. The first project concerns the activity of mTOR in mitochondrial function. We have recently found that FKBP38 is involved in recruitment of mTOR to mitochondria. The project investigates the role of the mitochondrial localized mTOR in mitochondrial function and cell senescence. The second project aims at the mechanism of FKBP38 in apoptosis regulation. FKBP38 has been shown to interact with the anti-apoptotic proteins, Bcl-2 and Bcl-xL. The project is to determine whether nutrient, growth factor and oxygen levels control the anti-apoptotic activity of Bcl-2 and Bcl-xL through FKBP38. The third project focuses on the role of primary cilium in mTOR regulation. Primary cilium is a vital cellular organelle that functions as a signaling hub in many eukaryotic cells. mTOR has been recently found to be a key effector of primary cilium-mediated signaling. This project explores the mechanisms through which primary cilium controls mTOR activity.