Elevated levels of reactive oxygen species (ROS) are associated with cell damage and dysfunction and have been implicated in the progression of numerous neurodegenerative disorders. Mechanisms that limit cellular ROS accumulation, and thereby prevent oxidant-induced damage, have been elucidated. However, many questions remain as to how cells cope with oxidant-induced damage that can occur when the levels of cellular ROS exceed the capacity of these anti-oxidant systems.

Research in the Sevier lab focuses on the identification and characterization of pathways used by cells to sense and respond to cellular redox imbalances. We are particularly interested in the redox-signaling events that act to maintain protein-folding homeostasis in the endoplasmic reticulum and cytoplasm during excessively oxidizing conditions (during conditions of increased cellular ROS).

We study the molecular mechanisms regulating cellular oxidative folding and stress pathways using a combination of molecular, genetic, and biochemical techniques.