M
Masahiro Yamamoto
Researcher at Osaka University
Publications - 472
Citations - 36678
Masahiro Yamamoto 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 77, co-authored 434 publications receiving 33443 citations. Previous affiliations of Masahiro Yamamoto include Tokyo Medical and Dental University & National Institute of Radiological Sciences.
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Journal ArticleDOI
The E2-Like Conjugation Enzyme Atg3 Promotes Binding of IRG and Gbp Proteins to Chlamydia - and Toxoplasma -Containing Vacuoles and Host Resistance
TL;DR: It is shown that Atg3 expression, similar to Atg5 expression, is required for IRG and Gbp proteins to dock to PVs, and that IFN-induced cell-autonomous resistance to C. trachomatis infections in mouse cells depends not only on Atg 5 and IRG proteins, as previously demonstrated, but also requires the expression of Atg 3 and GBP proteins.
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Toll/IL-1 receptor domain-containing adaptor inducing IFN-beta (TRIF)-mediated signaling contributes to innate immune responses in the lung during Escherichia coli pneumonia.
Samithamby Jeyaseelan,Scott K. Young,Michael B. Fessler,Yuhong Liu,Kenneth C. Malcolm,Masahiro Yamamoto,Shizuo Akira,G. Scott Worthen +7 more
TL;DR: It is found that rapid activation of TRIF-dependent TLR4-mediated signaling cascade serves to augment pulmonary host defense against a Gram-negative pathogen.
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Amphipathic α-helices in apolipoproteins are crucial to the formation of infectious hepatitis C virus particles.
Takasuke Fukuhara,Masami Wada,Shota Nakamura,Chikako Ono,Mai Shiokawa,Satomi Yamamoto,Takashi Motomura,Toru Okamoto,Daisuke Okuzaki,Masahiro Yamamoto,Izumu Saito,Takaji Wakita,Kazuhiko Koike,Yoshiharu Matsuura +13 more
TL;DR: Results suggest that amphipathic α-helices in the exchangeable apolipoproteins play crucial roles in the infectious particle formation of HCV and provide clues to the understanding of life cycle ofHCV and the development of novel anti-HCV therapeutics targeting for viral assembly.
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Viral Replication Complexes Are Targeted by LC3-Guided Interferon-Inducible GTPases.
Scott B. Biering,Jayoung Choi,Rachel A. Halstrom,Hailey M. Brown,Wandy L. Beatty,Sanghyun Lee,Broc T. McCune,Erin Dominici,Lelia E. Williams,Robert C. Orchard,Craig B. Wilen,Masahiro Yamamoto,Jörn Coers,Gregory A. Taylor,Seungmin Hwang +14 more
TL;DR: It is shown that interferon-gamma (IFNG) disrupts the RC of murine norovirus (MNV) via evolutionarily conserved autophagy proteins and the induction of IFN-inducible GTPases, which are known to destroy the membrane of vacuoles containing bacteria, protists, or fungi.
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Essential role for GABARAP autophagy proteins in interferon-inducible GTPase-mediated host defense.
Miwa Sasai,Naoya Sakaguchi,Ji Su Ma,Shuhei Nakamura,Tsuyoshi Kawabata,Hironori Bando,Youngae Lee,Tatsuya Saitoh,Shizuo Akira,Akiko Iwasaki,Daron M. Standley,Tamotsu Yoshimori,Masahiro Yamamoto +12 more
TL;DR: This work shows a unique role of GABARAPs, in particular gamma-aminobutyric acid (GABA)-A-receptor-associated protein-like 2 (Gabarapl2; also known as Gate-16), in interferon-γ (IFN-γ)-mediated antimicrobial responses.