| Project/Area Number |
16300151
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biomedical engineering/Biological material science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MIYAGISHI Makoto The University of Tokyo, Faculty of Medicine, Project Associate Professor, 医学部附属病院, 特任助教授 (30323538)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥14,300,000 (Direct Cost: ¥14,300,000)
Fiscal Year 2005: ¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 2004: ¥9,300,000 (Direct Cost: ¥9,300,000)
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| Keywords | Interferon Response / RNA interference / Biotechnology / siRNA / ジーンディスカバリー / アポトシス / RNAiライブラリー |
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| Research Abstract |
In mammalian cells, siRNAs have been used to induce RNA interference (RNAi) in an attempt to prevent nonspecific effects (including the interferon (IFN) response) which are caused by long double-stranded RNAs (dsRNAs) of more than 30 bp. In this project, we developed a novel and simple strategy for avoiding activation of the IFN response by dsRNA, and analyzed interferon pathway by means of siRNA library. We showed that modified hairpin-RNAs (mhRNAs) of more than 100 bp, with multiple specific point-mutations within the sense strand and transcribed from the U6 or tRNAVa1 promoters, can cause RNAi without inducing the IFN pathway genes. These findings should enhance the exploitation of RNAi in mammalian cells, especially in the field of RNAi therapy against pathogenic viruses. Furthermore the results from screening by siRNA library showed that apoptosis pathway induced by dsRNA include a JNK/SAPK-mediated mitochondrial pathway and an ERK2-related pathway.
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