Recent evidence suggests that the production of Reactive Oxygen Species (ROS) is tightly regulated and serves a physiological function during mitogenic stimulation of cultured cells. The research interest of this laboratory is to provide mechanistic understanding of the role intracellular redox-state plays in regulating the mammalian cell cycle, and establish a link between ROS-signaling and other aspects of intracellular signaling networks.
Research efforts are concentrated in identifying the molecular mechanisms involved in the regulation of the redox-sensitive G1-checkpoint following mitogenic stimuli and in asynchronously growing exponential cells. The possible role of ROS and thiol-redox reactions in regulating expression and activities of cyclins, CDKs, CKIs, CDC25, Rb, thioredoxin, and glutaredoxin are of immediate interests.
Research efforts are also ongoing investigating the possible role of intracellular antioxidants in radiosensitivity and radiation-induced cell cycle checkpoint pathways both in normal and tumor cells
Additional research interest includes possible role of intracellular redox-reactions in post-transcriptional (mRNA turnover) regulation of antioxidant enzymes and cell cycle checkpoint genes expression. Specifically, the possible role of redox-state in UTR RNA-protein binding and subsequent mRNA turnover are actively pursued. The knowledge gained from these research projects may provide novel insights into the regulation of the mammalian cell cycle both in physiological as well as pathological states. This knowledge may allow us to devise better treatment protocols based on redox control of the cell cycle.