Chihiro Sasakawa
Director, Professor
Microbiology and Immunology
Chiba University
Japan
Biography
Chihiro Sasakawa received his Ph. D. from the University of Tokyo in 1978. He was a postdoctoral fellow at Washington University, School of Medicine at St. Louis from 1980-1983. After return to Tokyo, he initiated studies on bacterial pathogenesis at the Institute of Medical Science, the University of Tokyo, and became a Professor in 1995. He served as the Head of Department of Microbiology and Immunology from 1999-2005. He became a Professor Emeritus of the University of Tokyo in 2012, and continuously dedicates not only to promote his own research but also participated in academia as a member of Science Council of Japan since 2010, the President of Federation of Microbiological Societies of Japan since 2010, and the Director of Medical Mycology Research Center at the Chiba University since 2013. He was nominated as a member of American Academy of Microbiology in 2014.
Research Interest
Study of bacterial infectious strategy and host innate immune response, and its application toward disease control.
Publications
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Kobayashi T, Ogawa M, Sanada T, Mimuro H, Kim M, Ashida H, Akakura R, Yoshida M, Kawalec M, Reichhart JM, Mizushima T, Sasakawa C. The Shigella OspC3 effector inhibits caspase-4, antagonizes inflammatory cell death, and promotes epithelial infection. Cell Host Microbe. 13(5):570-83, 2013.
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Ashida H, Kim M, Sasakawa C. Exploitation of the host ubiquitin system by bacterial pathogens. Nat Rev Microbiol, 12(6): 399-413, 2014.
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Kiga K, Mimuro H, Suzuki M, Shinozaki-Ushiku A, Kobayashi T, Sanada T, Kim M, Ogawa M, Iwasaki YW, Kayo H, Fukuda-Yuzawa Y, Yashiro M, Fukayama M, Fukao T, Sasakawa C. Epigenetic silencing of miR-210 increases the proliferation of gastric epithelium during chronic Helicobacter pylori infection. Nat Communication, 5:4497, 2014.
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Suzuki S, Mimuro H, Kim M, Ogawa M, Ashida H, Toyotome T, Franchi L, Suzuki M, Sanada T, Suzuki T, Tsutsui H, Núñez G, Sasakawa C. Shigella IpaH7.8 E3 ubiquitin ligase targets glomulin and activates inflammasomes to demolish macrophages. Proc Natl Acad Sci USA. 111(40):E4254-63, 2014.
