I joined Genentech in 2001 as a postdoc after completing my PhD in the cell death lab of Andreas Strasser at the Walter & Eliza Hall Institute in Australia. As a postdoc with Vishva Dixit, I worked on several projects including the role of the adaptor protein CARMA1/CARD11 in lymphocyte development and activation, the effect of TNF family ligands EDA-A1 and EDA-A2 on hair, sweat gland and muscle homeostasis, and the characterization of a kinase called RIPK3, which turned out to be a key effector of a regulated form of necrotic cell death termed necroptosis. These diverse projects were developed in collaboration with several departments and I saw first hand how much can be achieved when experts across disciplines pull together. Enthusiastic, talented colleagues combined with exciting, medically relevant science made staying on as a scientist an easy decision.
The current mission of my group is to decipher the signaling mechanisms unleashing proinflammatory cell death programs that may exacerbate a range of inflammatory diseases. Our goal is to unveil novel therapeutics targets with the potential to benefit patients.
Nature. 2016 Dec 1;540(7631):129-133.
Inflammation is a driving factor in many chronic diseases. My group studies the contribution of cell death to inflammation because dying cells can release molecules that activate innate immune cells to produce an inflammatory response. Recent work has focused on the kinases RIPK1 and RIPK3 because of their contribution to proinflammatory cell death. We are using genetic and biochemical approaches to understand how, when and where these kinases get activated, as well as the signaling mechanisms that normally hold these kinases in check.