Controlling HCV replication by targeting intracellular signaling
Project/Area Number |
21590843
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
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Research Institution | 独立行政法人国立病院機構大阪医療センター(臨床研究センター) (2011) Osaka University (2009-2010) |
Principal Investigator |
ISHIDA Hisashi 独立行政法人国立病院機構大阪医療センター(臨床研究センター), 研究員 (00506230)
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Co-Investigator(Kenkyū-buntansha) |
TAKEHARA Tetsuo 大阪大学, 大学院・医学系・研究科, 教授 (70335355)
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Project Period (FY) |
2009 – 2011
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Project Status |
Completed (Fiscal Year 2011)
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Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | C型肝炎ウイルス / BCAA / ウイルス粒子形成 / mTOR / マイクロRNA / PI3キナーゼ |
Research Abstract |
In this study, we investigated factors affecting intracellular signaling which could control HCV replication. Among microRNAs which were regulated by HCV infection, miR192/miR-215 and miR-491 were identified as the factors which could regulate HCV replication. miR-491 was demonstrated to suppress PI3 kinase/Akt pathway, responsible for HCV augmentation. Branched-chain amino acids could suppress HCV RNA replication whereas enhance HCV particle formation, which suggested some signaling regulated by BCAA may be involved in controlling HCV replication.
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Report
(4 results)
Research Products
(8 results)
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[Journal Article] Alterations in microRNA expression profile in HCV-infected hepatoma cells : involvement of miR-491 in regulation of HCV via the PI3 kinase/Akt pathway2011
Author(s)
Ishida H, Tatsumi T, Hosui A, Nawa T, Kodama T, Shimizu S, Hikita H, Hiramatsu N, Kanto T, Hayashi N, Takehara T
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Journal Title
Biochem Biophys Res Commun
Volume: Vol.412
Pages: 92-97
Related Report
Peer Reviewed
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