Molecular interaction between intracellular detection of viral RNAs and stress responses
| Project/Area Number |
18H02660
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 49060:Virology-related
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| Research Institution | Chiba University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2020: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2018: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
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| Keywords | ウイルス / 自然免疫 / ストレス応答 / RNA結合タンパク質 / RNA / ウイルス感染 |
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| Outline of Final Research Achievements |
In this study, we tried to understand the relationship between the innate immune responses triggered by the intracellular viral infection sensors, RIG-I-like receptors (RLRs), and the stress responses regulated by the antiviral stress granules (avSG), which are formed by sensing infection as stresses. We focused on the RNA-binding proteins (RBPs) that are commonly involved in these two responses. We identified RBPs localized in avSG in response to viral infection and involved in positive and negative regulation of antiviral defenses.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、ウイルス感染に応答した抗ウイルス自然免疫応答と、翻訳抑制へとつながるストレス応答に共通する制御機構を解析し、そこに関与するRBPの同定とそれによる生体防御の制御機構を明らかにした。ここから得られた知見は、２つのストレス応答による細胞の恒常性維持機構の分子メカニズムの理解につながるだけでなく、ウイルス感染症やストレス関連疾患に対する新たな治療戦略につながる知見へとつながる可能性がある。
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Report
(4 results)
Research Products
(16 results)
