研究者業績

尾野 本浩司

オノモト コウジ  (KOJI ONOMOTO)

基本情報

所属
千葉大学 真菌医学研究センター 助教
学位
理学博士(早稲田大学)

J-GLOBAL ID
201801011703354076
researchmap会員ID
B000322691

論文

 37
  • Keiko Shibata, Harune Moriizumi, Koji Onomoto, Yuka Kaneko, Takuya Miyakawa, Shuhei Zenno, Masaru Tanokura, Mitsutoshi Yoneyama, Tomoko Takahashi, Kumiko Ui-Tei
    Nucleic Acids Research 2024年4月19日  
    Abstract RNA silencing is a post-transcriptional gene-silencing mechanism mediated by microRNAs (miRNAs). However, the regulatory mechanism of RNA silencing during viral infection is unclear. TAR RNA-binding protein (TRBP) is an enhancer of RNA silencing that induces miRNA maturation by interacting with the ribonuclease Dicer. TRBP interacts with a virus sensor protein, laboratory of genetics and physiology 2 (LGP2), in the early stage of viral infection of human cells. Next, it induces apoptosis by inhibiting the maturation of miRNAs, thereby upregulating the expression of apoptosis regulatory genes. In this study, we show that TRBP undergoes a functional conversion in the late stage of viral infection. Viral infection resulted in the activation of caspases that proteolytically processed TRBP into two fragments. The N-terminal fragment did not interact with Dicer but interacted with type I interferon (IFN) signaling modulators, such as protein kinase R (PKR) and LGP2, and induced ER stress. The end results were irreversible apoptosis and suppression of IFN signaling. Our results demonstrate that the processing of TRBP enhances apoptosis, reducing IFN signaling during viral infection.
  • Im JH, Duic I, Yoshimizu SH, Onomoto K, Yoneyama M, Kato H, Fujita T
    Scientific Reports 13(1) 6318 2023年4月  査読有り
  • Isshu Kojima, Koji Onomoto, Wenjie Zuo, Makoto Ozawa, Kosuke Okuya, Kiyotada Naitou, Fumiki Izumi, Misuzu Okajima, Takuro Fujiwara, Naoto Ito, Mitsutoshi Yoneyama, Kentaro Yamada, Akira Nishizono, Makoto Sugiyama, Takashi Fujita, Tatsunori Masatani
    Journal of Virology 2022年9月7日  
    Rabies virus (RABV) is a neglected zoonotic pathogen that causes lethal infections in almost all mammalian hosts, including humans. Recently, RABV has been reported to induce intracellular formation of stress granules (SGs), also known as platforms that activate innate immune responses.
  • 尾野本浩司, 米山光俊, 浅倉聡, 浅倉聡, 松本伸一, 海宝龍夫, 海宝龍夫
    日本防菌防黴学会誌 50(3) 2022年  
  • Koji Onomoto, Kazuhide Onoguchi, Mitsutoshi Yoneyama
    Cellular & molecular immunology 18(3) 539-555 2021年3月  
    Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are RNA sensor molecules that play essential roles in innate antiviral immunity. Among the three RLRs encoded by the human genome, RIG-I and melanoma differentiation-associated gene 5, which contain N-terminal caspase recruitment domains, are activated upon the detection of viral RNAs in the cytoplasm of virus-infected cells. Activated RLRs induce downstream signaling via their interactions with mitochondrial antiviral signaling proteins and activate the production of type I and III interferons and inflammatory cytokines. Recent studies have shown that RLR-mediated signaling is regulated by interactions with endogenous RNAs and host proteins, such as those involved in stress responses and posttranslational modifications. Since RLR-mediated cytokine production is also involved in the regulation of acquired immunity, the deregulation of RLR-mediated signaling is associated with autoimmune and autoinflammatory disorders. Moreover, RLR-mediated signaling might be involved in the aberrant cytokine production observed in coronavirus disease 2019. Since the discovery of RLRs in 2004, significant progress has been made in understanding the mechanisms underlying the activation and regulation of RLR-mediated signaling pathways. Here, we review the recent advances in the understanding of regulated RNA recognition and signal activation by RLRs, focusing on the interactions between various host and viral factors.

MISC

 28

書籍等出版物

 7

講演・口頭発表等

 6

共同研究・競争的資金等の研究課題

 8