| Project/Area Number |
10670407
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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 |
内科学一般
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| Research Institution | University of Tokyo |
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Principal Investigator |
KITANI Seiichi The Health Service Center, University of Tokyo, 保健管理センター, 助手 (10231284)
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| Co-Investigator(Kenkyū-buntansha) |
KOSHINO Takeshi Department of Pulmonary Medicine, University of Tokyo, 大学院・医学系研究科・呼吸器内科, 助手 (10282659)
MORITA Yutaka Department of Pulmonary Medicine, University of Tokyo, 大学院・医学系研究科・呼吸器内科, 助教授 (60107620)
TESHIMA Reiko Division of Biochemistry and Immunochemistry, National Institute of Health Sciences, 主任研究官 (50132882)
木原 英利 東京大学, 医学部付属病院, 医員
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1998: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Ectokinase / K252b / mast cells / アレルギー |
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| Research Abstract |
We examined the effects of K252b, an ectoprotein kinase inhibitor, on the activation process of RBL-2H3 cells by cross-linking of IgE receptors. Analysis of phosphorylation revealed that K252b inhibited the phosphorylation of a 130-kDa protein. K252b inhibited IgE-mediated degranulation from RBL-2H3 cells and human basophils and the sustained increase in the cytosolic calcium ion concentration even after addition of antigen.
To study the properties of the ectokinase activity on the outer cell surfaces of RBL-2H3 cells, we tested the several protein substrates. Casein and casein kinase II peptide were the most strongly phosphorylated. The phosphorylation was almost completely inhibited by K252b. These findings suggest that the effects of K252b may be mediated by outer surface ectokinase on mast cell, which is new target to suppress allergic inflammation.
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