Sahezeel Awadia received his PhD from the University of Toledo and joined the Rehemtulla laboratory in 2019. His current research is focused on delineating the structural and functional underpinnings for the role of FADD in regulating the APC/C complex during the G1 to S transition. In normal cells, the eukaryotic cell cycle is initiated by the binding of growth factors to cell surface transmembrane receptors, events that activate intracellular signaling pathways that promote cell growth and orderly entry into the four consecutive phases of cell division: G1, S, G2 and M. During G1-phase of the cell cycle, the decision for a cell to enter a state of quiescence, or commit to a cell cycle round by passing the restriction point (R-point) and enter the S-phase (when DNA replication is initiated) in response to growth factors is made based on a complex set of interactions between cyclin-dependent kinases (Cdks), Cdk inhibitors (CKIs), and the anaphase-promoting complex/cyclosome (APC/C). Unlike normal cells, cancer cells evolve the ability to evade the R-point and continue through the cell cycle and overcome the R-point, even in the absence of extracellular growth factors and despite the presence of extensive DNA damage. The Rehemtulla lab has identified FADD (Fas Associated Death Domain), a protein commonly associated with apoptotic cell death, as a key mediator of the G1 to S transition. Dr. Awadia's recent work has identified FADD as a requisite regulator of the APC/C complex, wherein it functions as an APC/C inhibitor during the G1 to S transition. Normal as well as cancer cells lacking in FADD fail to overcome the R-point and remain arrested in G1 despite the presence of mitogenic proliferative signaling due to APC/C hyperactivation.