2002 Fiscal Year Final Research Report Summary
Functional Regulation of Cell Adhesion Molecules by Neural Specific Carbohydrate
| Project/Area Number |
13680688
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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 |
Structural biochemistry
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
OKA Shogo Grad. Sch. Pharm. Sci., Kyoto U., Associate Professor, 薬学研究科, 助教授 (60233300)
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| Co-Investigator(Kenkyū-buntansha) |
KAWASAKI Toshisuke Grad. Sch. Pharm. Sci., Kyoto U., Professor, 薬学研究科, 教授 (50025706)
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| Project Period (FY) |
2001 – 2002
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| Keywords | HNK-1 carbohydrate / glucuronyltransferase / cell adhesion molecule / gene-deficient mice / long-term potentiation / water maze test |
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| Research Abstract |
The HNK-1 carbohydrate is characteristically expressed on a series of cell adhesion molecules and also on some glycolipids in the nervous system. The HNK-1 carbohydrate thought to be involved in cellcell and/or cellsubstrate interaction and recognition during the development of the nervous system. The characteristic structural feature of this carbohydrate is the sulfoglucuronyl residue, because the inner structure, Gal β1-4 GlcNAc, is found commonly in various glycoproteins and glycolipids. We cloned novel glucuronyltransferases (GlcAT-P and GlcAT-S), which are key enzymes involved in the biosynthesis of this carbohydrate. We have recently generated mice with a targeted deletion of the GlcAT-P gene. In the present study, we obtained following results using the GlcAT-P deficient mice. 1) The GlcAT-P deficient mice exhibited normal development of gross anatomical features but the adult mutant mice exhibited reduced longterm potentiation (LTP) at the Schaffer colIateral-CA1 synapses and defect in spatial memory formation. 2) In GlcAT-P deficient mice, the HNK-1 carbohydrate disappeared almost completely but a trace of HNK-1 immunoreactivity remained on the surfaces of soma and proximal dendrites of a subset of neurons in some limited regions. The remaining HNK-1 carbohydrate in the GlcAT-P deficient mice is synthesized by enzyme(s) other than GlcAT-P, presumably GlcAT-S
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Research Products
(10 results)
