| Project/Area Number |
15K06926
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
System genome science
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| Research Institution | Ritsumeikan University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
西澤 幹雄 立命館大学, 生命科学部, 教授 (40192687)
稲葉 宗夫 関西医科大学, 医学部, 非常勤講師 (70115947)
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| Co-Investigator(Renkei-kenkyūsha) |
YOSHIDA Noriyuki 立命館大学, 薬学部, 助教 (10363996)
JIANG Shiwen (ODAKA Tokifumi) 関西医科大学, 医学部, 助教 (10548746)
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| Research Collaborator |
SAKAMOTO Ryou
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 制御性RNA / タンパク質非コード性RNA / アンチセンスRNA / 遺伝子発現制御 / Proof-of-Concept実験 / Natural antisense RNA / インフルエンザウイルス感染 / POC実験 / microRNA / competing endogenous RNA / ceRNA network / EphA2 / RNAseq / RIP-RNAseq / RIP-RT PCR / 抗ヒトAgo2抗体 / 抗ヒトHuR抗体 / ヒトインフルエンザウイルス感染 / natural antisense RNA / ceRNA ネットワーク / RNA-seq法 / ヒトAgo2抗体 / RISC / IFN-alpha1 antisense RNA |
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| Outline of Final Research Achievements |
We reported a natural antisense (AS) RNA as an important modulator of IFN-α1 mRNA levels. We showed that IFN-α1 AS promotes IFN-α1 mRNA stability by transient duplex formation and inhibition of miR-1270-induced mRNA decay. Here, we performed a proof-of-concept experiment to verify the AS-mRNA regulatory axis exerts in vivo control over the expression of innate immunity by the proposed actions of IFN-α1 AS. We established a guinea pig model system for influenza virus infection, which encodes a functional MX1 gene, an important antiviral effector in the type I IFN pathway. This system allowed us to investigate the effects of antisense oligoribonucleotides (asORNs) representing functional domains of guinea pig IFN-α1 AS on gpIFN-α1 mRNA levels and, consequently, on viral proliferation in the respiratory tract of influenza virus A-infected animals. The results indicate that, in light of the proposed actions, the asORNs may modulate the level of IFN-α1 mRNA expression in vivo.
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