Functional roles of SV40 microRNA in host antiviral immunity.
| Project/Area Number |
25460075
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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 |
Biological pharmacy
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| Research Institution | Musashino University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAHASHI TETSUYUKI 武蔵野大学, 薬学研究所, 講師 (00403692)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | マイクロRNA / SV40 / 炎症性サイトカイン / DNA複製 / miR-S1 / SV40ウイルス / T抗原 / VP1 / マイクロＲＮＡ / ＳＶ４０ / シード配列 |
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| Outline of Final Research Achievements |
We explored functional roles of miR-S1 encoded by SV40 virus in DNA replication and cytokine expression within HEK293 cells transfected with SV40 genome vectors. Semi-quantitative qPCR analysis showed that miR-S1-3p rather than miR-S1-5p was more abundantly expressed in cells transfected with SV40 genome vectors. Consistently, reporter assays showed that miR-S1-3p had much more repressive effects on luciferase activity than miR-S1-5p did. Replication rate of viral DNA were evaluated by qPCR analysis in various types of cells transfected with SV40 vectors with or without miR-S1 expression. These results indicated that the replication rate increased proportionally to T antigen expression, but was retarded by its excess expression, often observed in transfected cells without miR-S1 expression. Examination of cytokine expressions in HEK293 cells transfected with SV40 vectors revealed that miR-S1 affected the expression of TNFalpha and IL17F through its modulation of T antigen expression.
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Report
(5 results)
Research Products
(3 results)
