Reuben Shaw, PhD

The central focus of my laboratory at the Salk Institute is the AMPK signaling pathway and understanding how it coordinates metabolism and growth across all eukaryotic species. AMPK is one of a handful of master regulators of metabolism which has been demonstrated to control aging and lifespan across multiple species. My laboratory works heavily in mammalian cells and in genetic engineered mice, studying metabolic disease and cancer predisposition. Previously, we demonstrated that the type 2 diabetes drug metformin requires LKB1 to activate AMPK in mouse liver and that liver-specific LKB1 knockout mice exhibit profound defects with elevated gluconeogenesis and lipogenesis. We have also studied the role of this pathway in different genetic mouse models of cancer. Most importantly, during the past 5 years, my lab has made the greatest impact in discovering and published a number of papers detailing analysis of many novel substrates of AMPK that mediate its effects on metabolism, cell growth, autophagy, and lifespan: raptor, Cry1, Srebp1, ULK1, Mitochondrial Fission Factor (MFF) and the Class IIa family of HDACs (HDAC4, HDAC5, HDAC7, and HDAC9).