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.
Papers
More filters
Book ChapterDOI
Lipid A receptor TLR4-mediated signaling pathways.
Masahiro Yamamoto,Shizuo Akira +1 more
TL;DR: This chapter discusses the mechanisms of the activation or de-activation program mediated by the Lipid A receptor TLR4, which is elaborately down-regulated by a number of negative regulators.
Journal ArticleDOI
Essential Roles of K63-Linked Polyubiquitin-Binding Proteins TAB2 and TAB3 in B Cell Activation via MAPKs
Daisuke Ori,Hiroki Kato,Hideki Sanjo,Sarang Tartey,Sarang Tartey,Takashi Mino,Shizuo Akira,Osamu Takeuchi,Osamu Takeuchi +8 more
TL;DR: It is demonstrated that TAB2 and TAB3 are essential for B cell activation leading to Ag-specific Ab responses, as well as B-1 and marginal zone B cell development, and that Tab2- and Tab3-mediated K63-linked polyubiquitin recognition controls B cellactivation via MAPKs, but not the TAK1/NF-κB axis.
Journal ArticleDOI
NF-IL6 represses early gene expression of human papillomavirus type 16 through binding to the noncoding region.
Satoru Kyo,Masaki Inoue,Yukihiro Nishio,Kazuyoshi Nakanishi,Shizuo Akira,Hirokazu Inoue,Masuo Yutsudo,Osamu Tanizawa,Akira Hakura +8 more
TL;DR: It is demonstrated that the nuclear factor for interleukin 6 expression (NF-IL6) specifically binds to the HPV16 NCR and represses the early gene expression of HPV16 and indicates that repression may be caused by competition with other transcriptional activators, such as NF-I and AP1.
Journal ArticleDOI
MyD88- and Bruton’s Tyrosine Kinase-Mediated Signals Are Essential for T Cell-Independent Pathogen-Specific IgM Responses
TL;DR: The results suggest that MyD88 specifically promotes T cell-independent BCR signaling and that, in the absence of Btk, this TLR-mediated stimulation is a required component of this signal.
Journal Article
Regulation of innate immune responses by Toll-like receptors.
Kiyoshi Takeda,Shizuo Akira +1 more
TL;DR: Progress in elucidating the molecular mechanisms for LPS tolerance has been made through the analysis of TLR-mediated signaling pathways, and an MyD88-independent pathway is now being characterized.