James Spudich

PhD in Biochemistry (Stanford University)

Over the last several decades the Spudich laboratory studied the structure and function of the myosin family of molecular motors in vitro and in vivo, and we developed multiple new tools, including in vitro motility assays taken to the single molecule level using laser traps. That work led us to our current focus on the human cardiac sarcomere and the molecular basis of hypertrophic and dilated cardiomyopathy. We postulated in 2015 that a majority of hypertrophic cardiomyopathy mutations are likely to be shifting b-cardiac myosin heads from a sequestered off-state to an active on-state for interaction with actin, resulting in the hypercontractility seen clinically in hypertrophic cardiomyopathy patients. This hypothesis is different from earlier prevailing views, and this viewing an old disease in a new light is the basis of our current research.