研究者データベース

應田 涼太(オウダ リヨウタ)
医学研究院 病理系部門 微生物学免疫学分野
助教

基本情報

所属

  • 医学研究院 病理系部門 微生物学免疫学分野

職名

  • 助教

学位

  • 生命科学博士(京都大学)

科研費研究者番号

  • 90817321

J-Global ID

研究キーワード

  • 自然免疫   

研究分野

  • ライフサイエンス / 免疫学

職歴

  • 2018年07月 - 現在 北海道大学 医学研究院 助教
  • 2017年04月 - 2018年06月 京都大学 ウイルス・再生医科学研究所 研究員
  • 2014年04月 - 2017年03月 米国立衛生研究所 研究員
  • 2013年04月 - 2014年03月 京都大学 ウイルス研究所 日本学術振興会 特別研究員

学歴

  • 2008年04月 - 2013年03月   京都大学 大学院   生命科学研究科

研究活動情報

論文

  • Takeuchi F, Ikeda S, Tsukamoto Y, Iwasawa Y, Qihao C, Otakaki Y, Ryota O, Yao WL, Narita R, Makoto H, Watashi K, Wakita T, Takeuchi K, Chayama K, Kogure A, Kato H, Fujita T
    PloS one 14 2 e0212233  2019年 [査読有り][通常論文]
  • Kamada R, Yang W, Zhang Y, Patel MC, Yang Y, Ouda R, Dey A, Wakabayashi Y, Sakaguchi K, Fujita T, Tamura T, Zhu J, Ozato K
    Proceedings of the National Academy of Sciences of the United States of America 2018年09月 [査読有り][通常論文]
  • Ryota Ouda, Naoyuki Sarai, Vishal Nehru, Mira C. Patel, Maxime Debrosse, Mahesh Bachu, Răzvan V. Chereji, Peter R. Eriksson, David J. Clark, Keiko Ozato
    FEBS Letters 592 10 1681 - 1692 2018年05月01日 [査読有り][通常論文]
     
    The role of the histone chaperone SPT6 in mammalian cells is not fully understood. Here, we investigated the involvement of SPT6 in type I interferon (IFN)-induced transcription in murine fibroblasts. In RNA-seq analysis, Spt6 siRNA attenuates about half of ~ 200 IFN-stimulated genes (ISGs), while not affecting housekeeping genes. ISGs with high mRNA induction are more susceptible to Spt6 siRNA than those with lower levels of induction. ChIP analysis shows that SPT6 is recruited to highly inducible, Spt6 siRNA-sensitive ISGs, but not to other siRNA-insensitive ISGs. Furthermore, SPT6 recruitment is abrogated in cells lacking the histone methyltransferase NSD2. In co-IP experiments, SPT6 interacts with NSD2. In summary, SPT6 facilitates IFN-induced transcription, highlighting its critical role in gene activation.
  • Nazmul Haque, Ryota Ouda, Keiko Ozato, J.Robert Hogg
    Nature Communication 9 1145 1145  2018年03月 [査読有り][通常論文]
  • Ruibo Li, Ryo Narita, Hiroshi Nishimura, Shinsuke Marumoto, Seiji P. Yamamoto, Ryota Ouda, Mitsuyoshi Yatagai, Takashi Fujita, Takashi Watanabe
    ACS Sustainable Chemistry and Engineering 6 1 119 - 126 2018年01月02日 [査読有り][通常論文]
     
    Pyroligneous acids (PA) from hardwood, softwood, and bamboo significantly disinfected encephalomyocarditis virus (EMCV). Twenty-five kinds of phenolic derivatives in the PAs were identified and quantified. The total amounts of phenolic compounds in bamboo PA is higher than those in the PAs from softwood and hardwood. Phenol, 2-methoxyphenol, 2-methoxy-4-methylphenol, and 2-methoxy-4-ethylphenol are the most abundant compounds in the PAs examined. The activities of all the phenolic compounds against the encephalomyocarditis virus were assessed. The number of phenolic hydroxyl groups significantly affects the antiviral activity, and catechol and its derivatives exhibit higher viral inhibition effects than other phenolic derivatives. In addition, substituents affect the antiviral activity of the compounds. Phenolic compounds with a methyl group show higher activities than with a methoxyl group (e.g., 2-methylphenol > 2-methoxyphenol). Moreover, the relative position of functional groups also plays a key role in the viral inhibition activity (e.g., 2,6-dimethoxyphenol > 3,4-dimethoxyphenol). Thus, PAs contain phenol derivatives with considerable structural diversity and viral inhibition activities, providing a new strategy for virus-inactivation treatment through the optimization of PA-derived phenol structures.
  • Li Ruibo, Narita Ryo, Ouda Ryota, Kimura Chihiro, Nishimura Hiroshi, Yatagai Mitsuyoshi, Fujita Takashi, Watanabe Takashi
    RSC ADVANCES 8 63 35888 - 35896 2018年 [査読有り][通常論文]
  • Ji-Seung Yoo, Kiyohiro Takahasi, Chen Seng Ng, Ryota Ouda, Koji Onomoto, Mitsutoshi Yoneyama, Janice Ching Lai, Simon Lattmann, Yoshikuni Nagamine, Tadashi Matsui, Kuniyoshi Iwabuchi, Hiroki Kato, Takashi Fujita
    PLOS PATHOGENS 10 3 e1004012  2014年03月 [査読有り][通常論文]
     
    RIG-I is a DExD/H-box RNA helicase and functions as a critical cytoplasmic sensor for RNA viruses to initiate antiviral interferon (IFN) responses. Here we demonstrate that another DExD/H-box RNA helicase DHX36 is a key molecule for RIG-I signaling by regulating double-stranded RNA (dsRNA)-dependent protein kinase (PKR) activation, which has been shown to be essential for the formation of antiviral stress granule (avSG). We found that DHX36 and PKR form a complex in a dsRNA-dependent manner. By forming this complex, DHX36 facilitates dsRNA binding and phosphorylation of PKR through its ATPase/helicase activity. Using DHX36 KO-inducible MEF cells, we demonstrated that DHX36 deficient cells showed defect in IFN production and higher susceptibility in RNA virus infection, indicating the physiological importance of this complex in host defense. In summary, we identify a novel function of DHX36 as a critical regulator of PKR-dependent avSG to facilitate viral RNA recognition by RIG-I-like receptor (RLR).
  • Ryota Ouda, Koji Onomoto, Kiyohiro Takahasi, Michael R. Edwards, Hiroki Kato, Mitsutoshi Yoneyama, Takashi Fujita
    JOURNAL OF BIOLOGICAL CHEMISTRY 286 29 26210 - U901 2011年07月 [査読有り][通常論文]
     
    In mammals, viral infections are detected by innate immune receptors, including Toll-like receptor and retinoic acid inducible gene I (RIG-I)-like receptor (RLR), which activate the type I interferon (IFN) system. IFN essentially activates genes encoding antiviral proteins that inhibit various steps of viral replication as well as facilitate the subsequent activation of acquired immune responses. In this study, we investigated the expression of non-coding RNA upon viral infection or RLR activation. Using a microarray, we identified several microRNAs (miRNA) specifically induced to express by RLR signaling. As suggested by Bioinformatics (miRBase Target Data base), one of the RLR-inducible miRNAs, miR-23b, actually knocked down the expression of very low density lipoprotein receptor (VLDLR) and LDLR-related protein 5 (LRP5). Transfection of miR-23b specifically inhibited infection of rhinovirus 1B (RV1B), which utilizes the low density lipoprotein receptor (LDLR) family for viral entry. Conversely, introduction of anti-miRNA-23b enhanced the viral yield. Knockdown experiments using small interfering RNA (siRNA) revealed that VLDLR, but not LRP5, is critical for an efficient infection by RV1B. Furthermore, experiments with the transfection of infectious viral RNA revealed that miR-23b did not affect post-entry viral replication. Our results strongly suggest that RIG-I signaling results in the inhibitions of infections of RV1B through the miR-23b-mediated down-regulation of its receptor VLDLR.

その他活動・業績

受賞

  • 日本インターフェロン・サイトカイン学会 優秀ポスター賞
     
    受賞者: 應田 涼太

教育活動情報

主要な担当授業

  • 基本医学研究
    開講年度 : 2020年
    課程区分 : 修士課程
    開講学部 : 医学院
    キーワード : 炎症、自然免疫系、獲得免疫系、抗原提示機能、MHC、がん免疫、腸管免疫、炎症性疾患 Inflammation, innate immunity, adaptive immunity, antigen presentation, MHC, cancer immunology, intestinal immunology, inflammatory disease
  • 基本医学総論
    開講年度 : 2020年
    課程区分 : 修士課程
    開講学部 : 医学院
    キーワード : 免疫学、自然免疫、獲得免疫、炎症、感染免疫、がん免疫 Immunology, innate Immunity, adaptive immunity, inflammation, infection immunity, cancer immunology
  • 医学総論
    開講年度 : 2020年
    課程区分 : 博士後期課程
    開講学部 : 医学院
    キーワード : 免疫学、自然免疫、獲得免疫、炎症、感染免疫、がん免疫 Immunology, innate immunity, adaptive immunity, inflammation, infection immunity, cancer immunology
  • 基盤医学研究
    開講年度 : 2020年
    課程区分 : 博士後期課程
    開講学部 : 医学院
    キーワード : 炎症、自然免疫系、獲得免疫系、抗原提示機能、MHC、がん免疫、腸管免疫、炎症性疾患 Inflammation, innate immunity, adaptive immunity, antigen presentation, MHC, cancer immunology, intestinal immunology, inflammatory disease
  • 微生物・免疫学実習
    開講年度 : 2020年
    課程区分 : 学士課程
    開講学部 : 医学部
    キーワード : 細菌、ウイルス、無菌操作、グラム染色、抗酸菌染色、培養、細胞培養、定量、抗生物質、CPE、PCR、ELISA、IFA、蛍光抗体法、抗体、ブロッティング、炎症性サイトカイン、フローサイトメトリー、リンパ球、マクロファージ
  • 免疫学
    開講年度 : 2020年
    課程区分 : 学士課程
    開講学部 : 医学部
    キーワード : 免疫学、自然免疫、獲得免疫、炎症、感染免疫、がん免疫


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