We wish to understand how non-canonical protein translation shapes the proteome and regulates cell fate decisions involving cell death and differentiation, specifically by studying the cap-independent translation factor DAP5 and its interacting partner PRRC2B.
A major focus of the lab has been to identify network interconnectivity, and to understand the significance of alternative death pathways. Of particular interest are nodes that have multi-modular functions that can be thought of as integration hubs that connect the various modules.
We have harnessed our new insights into the PCD network to understand the etiology of disease and to design cell death-based therapies for diseases involving perturbations of the network, such as cancer and inflammation.
