| Project/Area Number |
10672095
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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 |
医薬分子機能学
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| Research Institution | Science University of Tokyo |
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Principal Investigator |
IKEKITA Masahiko Science University of Tokyo Biological applied Science Professor, 理工学部, 教授 (70138981)
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| Co-Investigator(Kenkyū-buntansha) |
MAKINO Kimiko Science University of Tokyo Pharmaceutical Science Associate Professor, 薬学部, 助教授 (40147509)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2000: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | apoptosis / cell surface molecule / antigen / macrophage / lectin / sialic acid / sialidase / galactose / 細胞表層抗原 / 糖タンパク質 / アスパラギン結合型糖鎖 / 貧食 / ガレクチン |
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| Research Abstract |
Neutrophils undergo constitutive death by apoptosis, leading to safe nonphlogistic phagocytosis and clearance by macrophages.
I clarified next points in this research.
1)The fucose residues which bind the lactosamine structure were disappears with the induction of the potosis.
The sialic acid residures which bind with nonreducing end of glycoprotein sugar chain were released by activating sialidase.
2)That galactose residures were exposed by releasing the sialic acid of the nonreduction end.
3)The macrophage protein (the lectin molecule) recognized this exposed galactose residuesof the apoptotic cells.
3) It was recognized that the other recognition mechanism of the apoptotic cells. The phosphatidylserine which was a kind of the phospholipid in the inner cell membrane peculiarly appeared in the outer cell membrane in the apoptotic induction.
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