Studies on the development of allergy treatment using gene-knockout mice.
| Project/Area Number |
06650918
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
生物・生体工学
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| Research Institution | Okayama University |
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Principal Investigator |
OHMORI Hitoshi Professor Department of Biotechnology, Faculty of Engineering, Okayama University, 工学部, 教授 (70116440)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | gene targeting / Fc gamma receptor / gene-knockout mouse / allergy / anaphylaxy / IgG immune complex / B cells / mast cells / Fcガンマレセプター / 抗体 / 遺伝子ノックアウト / ES細胞 / 変異マウス / IgE抗体 / リンパ球 / IgG Fc受容体 / クラススイッチ / 遺伝子ターゲッティング / ノックアウトマウス |
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| Research Abstract |
The present research project is unique in that we attempted to develop technologies for the treatment of allergic diseases by focusing the role of Fc gamma receptor II (FcgammaRII). For this purpose, we established FcgammaRII-deficient mice by gene-targeting as follows. Targeting vector. A.2.65-kb BamHI fragment containing S1 and EC1 exon was replaced by a neo-resistant gene cassette. Homologous J1 ES cell recombinants were obtained at a frequency of 10.4%. Offsprings of heterozygous intercrosses were examined for the gene knockout by Southern blot of genomic DNA isolated from tail tips. It was found that one out of four offsprings possessed the homozygous disrupted gene in accordance with Mendelian frequency. Lack of FcgammaRII protein was confirmed on B cells, macrophages and mast cells by flow cytometry. Sensitivities of this animal to various allergic stimuli are being investigated.
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Report
(3 results)
Research Products
(5 results)
