Project/Area Number |
05660386
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Applied molecular and cellular biology
|
Research Institution | Gifu University |
Principal Investigator |
KISO Makoto Gifu University, Professor, 農学部, 教授 (90092931)
|
Co-Investigator(Kenkyū-buntansha) |
HASEGAWA Akira Gifu University, Professor, 農学部, 教授 (10026429)
ISHIDA Hideharu Gifu University, Assoc.Prof., 農学部, 助教授 (20203002)
|
Project Period (FY) |
1993 – 1994
|
Project Status |
Completed (Fiscal Year 1994)
|
Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1993: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
Keywords | sialyl-Lewis X / selectin / cell adhesion / sulpho-Lewis X / immunosuppression / ganglioside / sialic acid / シアリルルイスXガングリオシド / セレクチン-ファミリー / 機能性糖鎖 / 抗炎症剤 / 細胞接着 / 機能性オリゴ糖鎖 / シアリルLe^Xガングリオシド / ガングリオシドGM_4 / 1-デオキシノジリマイシン |
Research Abstract |
We have examined the molecular requirements of selectin recognition by use of a variety of synthetic carbohydrate analogues with specific modifications on the sialyl-Lewis X,a binding epitope of leukocyte-endothelial cell adhesion molecules (selectins). E- and L-Selectins require OH groups at c-2,3 and 4 of the L-fucose moiety, while p-selectin requires only oh-3. Modifications of the sialic acid moiety, except for the carboxyl group, have little effect on the binding of any of the selectins. All three selectins-bound efficiently to an sulpho-Lewis X analogue in which sialic acid and ceramide are replaced with the sulfate group and an artificial long-chain alkyl (B-30) , respectively. This molecule is now being examined for biomedical applications as an anti-inflammatory as well as anti-metastatic agent. It is of interest that a synthetic 2- (tetradecyl) hexadecyl 0- (5-acetamido-3,5-didoxy-D-glycero-alpha-D-galacto-2-nonulopyranosylonic acid) - (2-3) -0-beta-D-galactopyranosyl- (1-4) -beta-D-glucopyranoside, an analogue of ganglioside GM3, markedly inhibited the cellular immune response. This effect was quantitatively similar to that of cyclosporin A.
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