| Project/Area Number |
12470069
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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 |
Virology
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| Research Institution | Mie University |
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Principal Investigator |
ITO Yasuhiko Mie University, School of Medicine, Professor, 医学部, 教授 (00022872)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIO Machiko Mie University, School of Medicine, Assistant, 医学部, 助手 (70156040)
KAWANO Mitsuo Mie University, School of Medicine, lecture, 医学部, 講師 (00234097)
TSURUDOME Masato Mie University, School of Medicine, Associate Professor, 医学部, 助教授 (50159042)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥12,100,000 (Direct Cost: ¥12,100,000)
Fiscal Year 2002: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Paramyxoviridae / genus Rubulavirus / syncytium / CD147 / ADAM9 / monoclonal antibody / HIV / Osteoclast / パラミクソウイルス / FRP-1 / CD98 / 遺伝改変動物 / LAT-1 / ADAM / Cell fusion |
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| Research Abstract |
Virus-induced cell fusion is regulated by the interaction between virus-factors and cellular factors. Fusion regulatory protein-1(FRP-1), which is identical with CD98, plays an important role on regulation of virus-induced cell fusion. FRP-1 is a multi-functional molecule, that is, FRP-1 can enhance and suppress virus-induced cell fusion. We constructed FRP-1 transgenic mice and knockout mice. FRP-1 knockout mice were found to be lethal, indicating FRP-1 that FRP-1 is essential and indispensable to ontogeny. In this study, we clarified that ADAM9 and CD147 molecules co-operated with FRP-1 in regulation of virus-induced cell fusion and monocytes fusion. ADAM9 is scarcely expressed on the blood monocytes, and expression of ADAM9 is induced by treatment of monocytes with anti-FRP-1 monoclonal antibody. An anti-ADAM9 antibody enhanced FRP-1-mediated cell aggregation, while it blocked FRP-1-mediated cell fusion. New protein synthesis is necessary for the expression of ADAM9 and genistein suppresses induction of ADAM9. One antibody to CD147 enhanced, white another one suppressed HIV-mediated cell fusion. Furthermore, we analyzed function of FRP-1 light chain, and discovered the N-light chains, which show high homology to FRP-1 light chain. We determined the cell and tissue distribution of the light chains and N-light chains. In this study, we established new method regulating virus induced cell fusion.
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