| Project/Area Number |
09680616
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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 |
Functional biochemistry
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| Research Institution | Nagoya University |
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Principal Investigator |
MURAMATSU Hisako School of Medicine, Nagoya University Assistant Professor, 医学部, 助手 (50182134)
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| Co-Investigator(Kenkyū-buntansha) |
HABUSHI Osami Aichi University of Education, Faculty of Education, Professor, 教育学部, 教授 (90024067)
MURAMATSU Takashi School of Medicine, Professor, 医学部, 教授 (00030891)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | chondroitin 6-sulfate / sulfotransferase / gene knockout / N-acetylglucosamine / コンドロイチン硫酸 / ノックアウトマウス / ストローマ細胞 / 第9染色体 / FISH / コンドロイチン6-スルフォトランスフェラーゼ / マウス |
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| Research Abstract |
Genomic DNA of mouse chondroitin 6-sulfotransferase was used to construct targeting vector to delete the gene. Knockout mice devoid of chondroitin 6-sulfotransferase gene were born and could reproduce. Enzymatic assay confirmed the absence of the sulfotransferase activity in the knockout mice. Therefore, we concluded that chondroitin 6 sulfate is not necessary for development and reproduction. Possible abnormality of the knockout mice in immunological activities is under continued investigation. We found a mouse cDNA which has homology to chondroltin 6-sultotransferase and revealed that the new cDNA encoded elusive N-acetylglucosamine 6-sulfotransferase. The enzyme was involved in synthesis of 6-sulfo sialyl Lewis X structure, and was expressed in high endothelial venules of lymph nodes. Cotransfection of the cDNA and that of fucosyltransferase VII were able reconstitute functional L-selectin ligand on endothelial cells. To find out general function of 6-sulfo N-acetylglucosamine-containing structures, we are on the way to knockout the N-acetylglucosamine 6-sulfotransferase gene, again by isolating the gene and construction of the targeting vector.
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