Personal Statement

My expertise lies in the field of immunology, as well as in clinical and research gastroenterology and hepatology. The research group in my laboratory has expertise in using genetically modified animals and isolating primary cultured liver cells including hepatocytes, Kupffer cells and hepatic stellate cells. I received my residency and subsequent clinical training in GI-hepatobiliary surgery. After clinical training, I began my research career in a doctorate program in the immunology department. For my PhD, I studied toll-like receptor (TLR) 4 signaling-mediated inflammasome activation, including the activation of caspase-1, IL-1β, and IL-18 in Kupffer cells and in listeria infection, as well as TLR/myeloid differentiation 88 signaling in liver regeneration. In my postdoctoral training at Columbia University, I studied the role of TLR4 signaling in hepatic stellate cell activation and liver fibrosis. After my recruitment to the University of California, San Diego, I began independent research and extended my research field to the study of TLR2, 4 and 9 signaling and hepatocyte transforming growth factor-β signaling in alcoholic and nonalcoholic steatohepatitis. Recently, my group found that TAK1, an intracellular protein kinase, is a crucial molecule in preventing spontaneous hepatocyte death, liver inflammation, fibrosis and hepatocarcinogenesis. In addition, the follow-up study showed that hepatic TAK1 regulates autophagy in the development of fatty liver and liver cancer.

Contact the Seki Lab

8700 Beverly Blvd.
Davis Building, Rooms 2099, 2029
Los Angeles, CA 90048