| Project/Area Number |
61580159
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
物質生物化学
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| Research Institution | The Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
SUZUKI Akemi The Tokyo Mitropolitan Institute of Midical Science, 代謝研究室, 室長 (70134533)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Kyoko The Tokyo Mitropolitan Institute of Midical Science, 代謝研究室, 研究員 (30124481)
SUZUKI Minoru The Tokyo Mitropolitan Institute of Medical Science, 代謝研究室, 研究員 (40124466)
SEKINE Michiko The Tokyo Mitropolitan Institute of Midical Science, 代謝研究室, 研究員 (70124469)
HASHIMOTO Yasuhiro The Tokyo Mitropoliran Institute of Midecal Science, 代謝研究室, 研究員 (80164797)
NAKAMURA Yuri The Tokyo Mitropolitan Institute of Medical Science, 代謝研究室, 研究員 (10176373)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1987: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1986: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Genetic control / SSEA-1の発現制御 / 糖脂質発現の遺伝学 / 胎児分化抗原-1 / 糖脂質発現の遺伝学的解析 / マウス腎糖脂質 |
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| Research Abstract |
We have found the polymorphic difference in the expression of glycolipids in the kidney of inbred strains of mice. DBA/2 mice do not express GL-Y (Gal<beta>1-4(Fuc<alpha>1-3)Gicnac<beta> 1-6(Gal<beta>1-3)Gb4cel) but express GL-X (Gal<beta>1-3Gb4cer) and a single autosomal gene responsible for the defective GL-Y expression was identified by genetic analysis. This gene is suggested to encode a factor which is essential for tranferring GlcNAc onto Gal<beta> 1-3Gb4Cer and DBA/2 mice have a variation in this gene. Localizing this gene on a chromosome was achieved by the analysis on the recombinant inbred strains of BXD. Dr.Taylor in Jackson Laboratory suggested that the gene controlling GL-Y expression was closely linked to Ea-4 on chromosome 19. We have tried to set up an assay system for measuring GIcNAc transferase to produce GlcNAc-GL-X and it is almost completed. We have also found another polymorphic difference in ganglioside expression in the kidney. DBA/2 mice express Z1 (NeuGc<alpha>2-3GL-X) z2 (NeuGc<alpha>2-8NeuGc<alpha> 2-3GL-X) and this phenotype is recessive. The analysis on the genetic control of z1 and z2 expression indicated that a single autosomal gene is involved. In the backcross mice,z1 and z2 expression is always accompanied with the expression of G1-x but not with that of GL-Y. This evidence support a hypothesis i.e. a gene located near Ea-4 on chromosome 19 controls the expression of z1 and z2 as well as GL-Y.
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