| Project/Area Number |
18K15178
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 49070:Immunology-related
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| Research Institution | Saitama University (2019)
The University of Tokyo (2018) |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 自然免疫 / microRNA / RNAサイレンシング / ウイルスセンサー / LGP2 / TRBP / small RNA / 抗ウイルス応答 / マイクロRNA |
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| Outline of Final Research Achievements |
During viral infection, viral nucleic acids are detected by virus sensor proteins including toll-like receptor 3 or RIG-I-like receptors (RLRs) in mammalian cells. Activation of these virus sensor proteins induces type-I interferon production and represses viral replication. We reported that an RLR family member, LGP2, modulates RNA silencing by interacting with an RNA silencing enhancer, TRBP and LGP2 enhances apoptosis by upregulating apoptosis regulatory genes during viral infection via the interaction. Our findings may shed light on the mechanism of apoptosis, induced by the TRBP-bound miRNAs through the interaction of TRBP with LGP2, as an antiviral defense system in mammalian cells.
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| Academic Significance and Societal Importance of the Research Achievements |
この研究成果は、細胞内ウイルスセンサータンパク質が転写因子を活性化することで遺伝子発現を制御するだけでなく、microRNAを介したゲノムワイドな転写後遺伝子発現制御にも直接的に関与することを示す研究成果であり、ウイルス感染細胞におけるmicroRNAによる転写後遺伝子発現制御の重要性を示唆している。
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