Importance of Specification of RNA export pathway for HIV-1 gene expression
| Project/Area Number |
25460564
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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 | Kyoto University |
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Principal Investigator |
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ヒト免疫不全ウイルス / RNA核外輸送 / RNAスプライシング / RNA‐タンパク質複合体 / mRNA前駆体スプライシング |
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| Outline of Final Research Achievements |
Although intron-containing HIV-1 RNAs have the same features as cellular general mRNAs, HIV-1 blocks the utilization of mRNA export factor, TAP, during nuclear RNA export. The blockage was achieved by the activity of viral Rev protein to inhibit TAP recruitment to viral RNAs. However, why Rev inhibits the recruitment remains a mystery.
Since viral RNAs are exported without being spliced, Rev may block TAP recruitment to escape the commitment to RNA splicing. I hypothesized that TAP stimulates RNA splicing.
To test the hypothesis, we performed in vitro splicing assay. Splicing products were increased when purified recombinant TAP protein was added. Conversely, RNA splicing was delayed by TAP inhibitor. These results support the hypothesis that TAP stimulates RNA splicing.
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Report
(4 results)
Research Products
(10 results)
