Hayley Muendlein

I am fascinated with the idea of shifting the dogmas of cell death and discovering the intricate connections and crosstalk that are yet to be uncovered. Equipped with this interest, my work has led to the identification of novel functions for two key cell death effectors: RIPK1 and cFLIP. My current research continues to focus on the role of these proteins and their interacting partners in cell death and inflammatory signaling pathways. Specifically, I have demonstrated that ZBP1, previously studied only in the context of viral infection, is constitutively bound to RIPK1 and regulates cell death in response to bacterial lipopolysaccharide. Through these advances, we are beginning to build a clearer picture of the mechanisms that drive cell death under various conditions. However, our understanding of the physiological settings in which these cell death mechanisms prevail remains poorly understood. For this reason, I am focused on applying these biochemical findings in vivo using endotoxin- and TNF-shock and Yersinia pseudotuberculosis infection mouse models to study how cell death protein interactions regulate host responses and survival.