| Project/Area Number |
13670309
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
SHIMOIKE Takashi National Institute of Infectious Diseases, VIROLOGY II, SENIOR SCIENTIST (90332361)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI TETSURO NATIONAL INSTITUTE OF INFECTIOUS DISEASES, VIROLOGY II, SECTION CHIEF (00250184)
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| Project Period (FY) |
2001 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Hepatitis C virus / IRES / Translational regulation / Capsid protein / protein-RNA interaction / コア蛋白質 / 蛋白質-RNA相互作用 / 宿主因子 / 蛋白質RNA相互作用 / キャプシド蛋白質 / キャプシドタンパク質 / タンパク質RNA相互作用 |
|---|
| Research Abstract |
We observed that hepatitis C virus (HCV) core protein specifically inhibits translation initiated by an HCV internal ribosome entry site (IRES). To investigate the mechanism by which down-regulation of HCV translation occurs, a series of mutations were introduced into the IRES element, as well as the core protein, and their effect on IRES activity examined in this study. We found that expression of the core protein inhibits HCV translation possibly by binding to a stem-loop IIId domain, particularly a GGG triplet within the hairpin loop structure of the domain, within the IRES. Basic-residue clusters located at the N-terminus of the core protein have an inhibitory effect on HCV translation, and at least one of three known clusters is required for inhibition. We propose a model in which competitive binding of the core protein for the IRES and 40S ribosomal subunit regulates HCV translation.
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