| Project/Area Number |
23590543
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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 |
Virology
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| Research Institution | Kobe University |
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Principal Investigator |
DENG Lin 神戸大学, 医学(系)研究科(研究院), 助教 (40437497)
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| Co-Investigator(Kenkyū-buntansha) |
HOTTA Hak 神戸大学, 大学院医学研究科, 教授 (40116249)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | C型肝炎ウイルス / 発癌 / NS5A / SMYD3 / AGR3 / 感染症 / 癌化 / Ｃ型肝炎ウイルス / シグナル |
|---|
| Research Abstract |
Hepatitis C Virus (HCV) NS5A is a multifunctional protein involved in HCV life cycle and HCV-induced liver pathologies. To elucidate the role of NS5A in HCV pathogenesis, we searched for host proteins interacting with NS5A by tandem affinity purification and identified a novel NS5A-interacting protein, SET and MYND domain-containing 3 (SMYD3), a histone methyltransferase involved in the proliferation of cancer cells. The interaction of NS5A with SMYD3 was confirmed by co-immunoprecipitation, proximity ligation assay, and confocal microscopy. NS5A predominately colocalized with SMYD3 in the cytoplasm. Moreover, the interaction between NS5A and SMYD3 transcriptionally activated AGR3, which is involved in breast, prostate and ovary tumorigenesis and belongs to the family of protein disulfide isomerases. Taken together, these data suggest that the interaction between NS5A and SMYD3 causes hepatocytic dysfunction through upregulation of AGR3 expression.
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