Vsevolod V. Gurevich and Tina M. Iverson labs
I study a protein that is a master regulator of signaling and the key player in deactivation of the largest group of receptors, G protein-coupled receptors, which are targeted by more than a third of clinically used drugs. This protein is called arrestin, and my research focuses on how arrestins make the choice between different cellular outcomes. For example, arrestin signaling can promote the activation of cellular pathways involved in cell proliferation in response to extracellular mitogens. Mitogens signal through receptors to cause cell division through activation of mitogen-activated protein kinase (MAPK) cascades, a process that results in cell growth. Recent work has shown that arrestins act as scaffolds for MAPK cascades. Scaffold proteins promote signaling by bringing all molecular components together and localizing them to a specific part of the cell. Arrestins bind MAPK cascades and localize them within the cell; however, the mechanism of arrestin scaffolding is poorly understood. My thesis research aims to characterize the arrestin-MAPK interactions to better understand how arrestin dictates signaling through MAPK cascades and controls cellular outcomes.