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Published Papers 【 display / non-display 】

Published Papers 【 display / non-display 】

• Analysis of the interaction between the ORF42 and ORF55 proteins encoded by Kaposi's sarcoma-associated herpesvirus.

  Kuriyama K, Watanabe T, Ohno S

  Archives of virology ( Springer Science and Business Media LLC )  169 ( 5 ) 98   2024.04 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• Lysosome-Associated Membrane Proteins Support the Furin-Mediated Processing of the Mumps Virus Fusion Protein.

  Ueo A, Kubota M, Shirogane Y, Ohno S, Hashiguchi T, Yanagi Y

  Journal of virology   94 ( 12 )   2020.06 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• A comparative epigenome analysis of gammaherpesviruses suggests cis-acting sequence features as critical mediators of rapid polycomb recruitment.

  Günther T, Fröhlich J, Herrde C, Ohno S, Burkhardt L, Adler H, Grundhoff A

  PLoS pathogens   15 ( 10 ) e1007838   2019.10 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• Both type I and type III interferons are required to restrict measles virus growth in lung epithelial cells.

  Taniguchi M, Yanagi Y, Ohno S

  Archives of virology     2019.02 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• S100a4 is secreted by alternatively activated alveolar macrophages and promotes activation of lung fibroblasts in pulmonary fibrosis

  Wei Zhang, Shinji Ohno, Beatrix Steer, Stephan Klee, Claudia A. Staab-Weijnitz, Darcy Wagner, Mareike Lehmann, Tobias Stoeger, Melanie Königshoff, Heiko Adler

  Frontiers in Immunology ( Frontiers Media S.A. )  9   1216   2018.06 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

  　View Summary

  Idiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease, characterized by damage of lung epithelial cells, excessive deposition of extracellular matrix in the lung interstitium, and enhanced activation and proliferation of fibroblasts. S100a4, also termed FSP-1 (fibroblast-specific protein-1), was previously considered as a marker of fibroblasts but recent findings in renal and liver fibrosis indicated that M2 macrophages are an important cellular source of S100a4. Thus, we hypothesized that also in pulmonary fibrosis, M2 macrophages produce and secrete S100a4, and that secreted S100a4 induces the proliferation and activation of fibroblasts. To prove this hypothesis, we comprehensively characterized two established mouse models of lung fibrosis: infection of IFN-γR-/- mice with MHV-68 and intratracheal application of bleomycin to C57BL/6 mice. We further provide in vitro data using primary macrophages and fibroblasts to investigate the mechanism by which S100A4 exerts its effects. Finally, we inhibit S100a4 in vivo in the bleomycin-induced lung fibrosis model by treatment with niclosamide. Our data suggest that S100a4 is produced and secreted by M2 polarized alveolar macrophages and enhances the proliferation and activation of lung fibroblasts. Inhibition of S100a4 might represent a potential therapeutic strategy for pulmonary fibrosis.

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Other Papers 【 display / non-display 】

Other Papers 【 display / non-display 】

• 麻疹ウイルスの複製に関わる新規宿主因子の同定

  伊藤美菜子, 岩崎正治, 竹田誠, 中村崇規, 柳雄介, 大野真治

  日本ウイルス学会学術集会プログラム・抄録集   60th   278   2012.10

   

  J-GLOBAL

• 麻疹ウイルス単一血溝型決定の分子基盤

  田原舞乃, BRINDLEY Melinda A, 福原秀雄, 酒井宏治, 大野真治, 駒瀬勝啓, ROTA Paul A, PLEMPER Richard K, 前仲勝実, 竹田誠

  日本ウイルス学会学術集会プログラム・抄録集   60th   282   2012.10

   

  J-GLOBAL

• 麻疹ウイルス感染認識におけるMDA5の果たす役割

  池亀聡, 竹田誠, 大野真治, 中津祐一郎, 柳雄介

  日本ウイルス学会学術集会プログラム・抄録集   57th   268   2009.10

   

  J-GLOBAL

• ポリメラーゼ遺伝子は麻疹ウイルスEdmonston株の弱毒化を担っている

  竹田誠, 大野真治, 田原舞乃, 白銀勇太, 柳雄介

  日本ウイルス学会学術集会プログラム・抄録集   56th   302   2008.10

   

  J-GLOBAL

• 麻疹ウイルスHタンパク質による受容体認識の構造基盤

  橋口隆生, 橋口隆生, 竹田誠, 田原舞乃, 池亀聡, 大野真治, 柳雄介

  日本ウイルス学会学術集会プログラム・抄録集   56th   124   2008.10

   

  J-GLOBAL

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Grant-in-Aid for Scientific Research 【 display / non-display 】

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• Grant-in-Aid for Scientific Research(C)

  Project Year: 2019.04  -  2022.03 

  Direct: 3,300,000 (YEN)  Overheads: 990,000 (YEN)  Total: 4,290,000 (YEN)

• Effects of mutations in HHV8 isolated form Miyakojima island, Okinawa, Japan

  Grant-in-Aid for Scientific Research(C)

  Project Year: 2019.04  -  2022.03 

  Investigator(s): Ohno Shinji 

  Direct: 3,300,000 (YEN)  Overheads: 4,290,000 (YEN)  Total: 990,000 (YEN)

  　View Summary

  Human herpes virus (HHV) 8 is responsible for the development of classical Kaposi's sarcoma (KS) development. Miyakojima island (Okinawa, japan) exhibits high incidence rate of KS and is prevalent with HHV8 which has unique amino acid residue substitutions. In this study, we evaluated the influences of the substitutions in ORF72 or ORF42 upon tumorigenecity. We evaluated the cell growth of ORF72 or ORF42 expressing cells. Unfortunately, the genes did not stimulate cell proliferation of the cells we used. Further, the substitutions seen in miyakojima HHV8 did not affect the cell growth. As for ORF42, we found that this protein binds to ORF55, and HHV8 which lacks ORF42 reduces virus particle production as compared to original HHV8.

• Grant-in-Aid for Scientific Research(C)

  Project Year: 2014.04  -  2017.03 

  Direct: 3,800,000 (YEN)  Overheads: 1,140,000 (YEN)  Total: 4,940,000 (YEN)

• Herpesvirus switching mechanism of gene regulation.

  Grant-in-Aid for Scientific Research(C)

  Project Year: 2014.04  -  2017.03 

  Investigator(s): Ohno Shinji 

  Direct: 3,800,000 (YEN)  Overheads: 4,940,000 (YEN)  Total: 1,140,000 (YEN)

  　View Summary

  We analyzed the viral gene regulation of gammaherpesvirus. The open reading frame (ORF) 35 protein was considered to be essential for the viral growth. However, we revealed that the protein was not essential, but plays an important role for the efficiency of the viral replication. In addition, ORF35 protein was necessary for reactivation from latent infection. We also analyzed the function of ORF31 protein. And the protein was revealed to regulate viral gene expression and we identified functional domain of ORF31. Host proteins which bind to ORF31 and regulate viral replication was searched, and we found candidates. We are currently studying about these proteins.

• Grant-in-Aid for Scientific Research on Innovative Areas

  Project Year: 2012.06  -  2017.03 

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• 2024.08