| Project/Area Number |
16K15258
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Experimental pathology
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| Research Institution | Okayama University |
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Principal Investigator |
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| Research Collaborator |
Yang Xu
Sun Cuiming
Gao Tong
Miyatake Hideyuki
Kondo Masayuki
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2018: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 感染症 / シグナル伝達抑制 / MAPKシグナル伝達 / ウイルス感染 / シグナル伝達 |
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| Outline of Final Research Achievements |
In this study, we clarified the mechanism of viral infection from the viewpoint of Ras-Raf-ERK / MAPK and its endogenous suppressor Spred2, and we challenged the antiviral strategy via ERK suppression by supplementation of Spred2. Activation of ERK-MAPK and viral infection were suppressed by Spred2 gene transfer. There was no difference in virus infection in Spred2 overexpressing mice, suggesting that the endogenous Spred2 is sufficient to inhibit the infection. Cell-penetrating Spred2 created in this study failed to inhibit ERK activation, however, supplementation of functional Spred2 protein may become a new antiviral drug.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究課題により、Spred2導入によるウイルス感染制御を確認できた。Spred2過剰発現マウスの検討から、健常時は生来発現するSpred2により必要な抑制系は作動していると考えられた。本研究により、ヒトインフルエンザ感染血清や肺線維症肺での解析も実施できた。これらの疾患時に、膜透過性ペプチドを付加した機能性Spred2タンパクを補充できれば、汎用性の高い新しい抗ウイルス薬となる可能性が示唆された。これらの臨床データをもとに、新たな抗ウイルス戦略が期待できた意義は大きい。
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