| Project/Area Number |
25460383
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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 |
Pathological medical chemistry
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| Research Institution | University of Fukui |
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Principal Investigator |
SADA Kiyonao 福井大学, 医学部, 教授 (10273765)
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| Co-Investigator(Kenkyū-buntansha) |
CHIHARA Kazuyasu 福井大学, 医学部, 准教授 (00314948)
TAKEUCHI Kenji 福井大学, 医学部, 助教(学内講師) (40236419)
YAMAUCHI Shota 福井大学, 医学部, 特命助教 (00728941)
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| Co-Investigator(Renkei-kenkyūsha) |
HOTTA Hak 神戸大学, 保健学研究科, 教授 (40116249)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | C型肝炎ウイルス / チロシンキナーゼ |
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| Outline of Final Research Achievements |
Hepatitis C virus (HCV) infects B lymphocytes and induces B cell lymphoma, in addition to chronic hepatitis and hepatocellular carcinoma. However, molecular mechanism for the pathogenesis of HCV infection-mediated disorders remains unclear. In this study, we investigated the role of protein-tyrosine kinases on HCV lifecycle, because HCV interacts with protein-tyrosine kinases in B cells. As a result, we found that HCV particle assembly involves phosphorylation of NS5A (non-structural protein of HCV) by the c-Abl protein-tyrosine kinase.
In parallel with this study, we investigated the molecular mechanism of infection immunity. We identified the novel mast cell anti-fungal immunity through Dectin-1 and Syk, and novel regulatory mechanism of Syk substrate 3BP2 (c-Abl SH3 domain-binding protein-2) in B cells.
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