Dr. Feng Shao graduated in chemistry from Peking University in 1996, obtained his PhD from University of Michigan, USA in 2003 and was a Damon Runyon Postdoctoral Research Fellow at Harvard Medical School until 2005 when he returned to China to be become an Assistant Investigator at NIBS. Promoted to Associate Investigator in 2009 and Full Investigator in 2012, he is currently the Deputy Director of NIBS. His research team has made many important contributions to our understanding bacterial pathogenesis, innate immunity and pyroptotic cell death. His group identified the cytosolic pattern recognition receptors for bacterial flagellin, bacterial lipopolysaccharide (LPS) and Rho-modifying bacterial toxins. For these discoveries Feng Shao received an International Early Career Award from the Howard Hughes Medical Institute and the Irving Sigal Young Investigator Award from the Protein Society of the USA. He has been elected a member of the Chinese Academy of Science, an Associate Member of European Molecular Biology Organization (EMBO), and a Fellow of the American Academy of Microbiology.
Feng Shao’s Lecture, which will focus on the molecular dissection of Pyroptosis, should be of interest to many Divisions in SLS and those interested in regulation of the immune system, the prevention and treatment of cancer, the response to bacterial infection and cell signalling mechanisms. Feng will initially describe his discovery that Caspase isoforms are cytosolic receptors for bacterial lipopolysaccharide (LPS) and explain how they activate pyroptosis-mediated defense mechanisms by cleaving the Gasdermin D (GSDMD) to induce its intrinsic membrane pore-forming activity. He will then demonstrate that the related family member GSDME recognises caspase-3, enabling it to activate the membrane pore-forming domain of GSDME to initiate the switch from apoptosis to pyroptosis. The role of GSDME in cancer will be discussed, based on his finding thatGsdme KO mice are protected from chemotherapy-induced tissue damage and weight loss. Together, his findings define pyroptosis as Gasdermin-mediated programmed necrotic cell death.