S
Shizuo Akira
Researcher at Osaka University
Publications - 1330
Citations - 344469
Shizuo Akira is an academic researcher from Osaka University. The author has contributed to research in topics: Innate immune system & Immune system. The author has an hindex of 261, co-authored 1308 publications receiving 320561 citations. Previous affiliations of Shizuo Akira include University of California, Berkeley & Wakayama Medical University.
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Journal ArticleDOI
Lethal encephalitis in myeloid differentiation factor 88-deficient mice infected with herpes simplex virus 1.
Daniel S. Mansur,Erna Geessien Kroon,Maurício Lacerda Nogueira,Rosa Maria Esteves Arantes,Soraia C. O. Rodrigues,Soraia C. O. Rodrigues,Shizuo Akira,Ricardo T. Gazzinelli,Ricardo T. Gazzinelli,Marco Antônio Campos +9 more
TL;DR: The results suggest that innate resistance to HSV-1 is mediated by MyD88 and may rely on activation of multiple TLRs, which are downstream to mediated TLR activation and essential for the production of inflammatory cytokines.
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The nuclear factor interleukin-6 (NF-IL6) and signal transducer and activator of transcription-3 (STAT-3) signalling pathways co-operate to mediate the activation of the hsp90beta gene by interleukin-6 but have opposite effects on its inducibility by heat shock.
TL;DR: The levels of the 90 kDa heat-shock protein (hsp90) and the activity of the hsp90beta gene promoter are increased in response to treatment by interleukin (IL)-6 and their interaction with its stress-mediated activation is discussed in terms of the multiple stimuli that may regulate the hSp90 promoter in unstressed cells.
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c‐Jun mediates hepatitis C virus hepatocarcinogenesis through signal transducer and activator of transcription 3 and nitric oxide–dependent impairment of oxidative DNA repair
Keigo Machida,Hidekazu Tsukamoto,Hidekazu Tsukamoto,Jian-Chang Liu,Yuan-Ping Han,Sugantha Govindarajan,Michael M. C. Lai,Shizuo Akira,Jing-hsiung James Ou +8 more
TL;DR: It is indicated that the HCV core protein potentiates chemically induced HCC through c‐Jun and STAT3 activation, which in turn, enhances cell proliferation, suppresses apoptosis, and impairs oxidative DNA damage repair, leading to hepatocellular transformation.
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Defective IL-2-mediated IL-2 receptor alpha chain expression in Stat3-deficient T lymphocytes.
Hiroshi Akaishi,Kiyoshi Takeda,Tsuneyasu Kaisho,Ryuzaburo Shineha,Susumu Satomi,Junji Takeda,Shizuo Akira +6 more
TL;DR: It is demonstrated that Stat3 activation is required for efficient T cell proliferation by IL-2 throughIL-2Ralpha induction, which is responsible for IL-1- and IL-6-induced proliferation through distinct mechanisms.
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Toxoplasma gondii Genotype Determines MyD88-Dependent Signaling in Infected Macrophages
TL;DR: It is suggested that RH triggers MAPK activation and IL-12 production using MyD88-independent signaling, whereas ME49 uses these pathways as well as MyD 88-dependent signaling cascades.