| Project/Area Number |
01480239
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Hospital of Medical School, Niigata University |
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Principal Investigator |
SATO Shuzo Hospital of Medical School, Department of Neurology, Lecturer, 医学部・附属病院・神経内科, 講師 (30115034)
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| Co-Investigator(Kenkyū-buntansha) |
MIYATAKE Tadashi Brain Research Institute, Department of Neurology, Professor, 脳研究所・神経内科, 教授 (50048998)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1990: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1989: ¥5,400,000 (Direct Cost: ¥5,400,000)
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| Keywords | Myelin / Myelin-associated glycoprotein / Cell adhesion molecule / Demyelination / Remyelination / Cell adhesion molecule / Demyclination / Remyclination / ミエリン / 糖蛋白 / Myelin-associated glycoprotein / cDNAクロ-ニング / 中大脳動脈結紮モデル / クプリゾン中毒 |
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| Research Abstract |
The myelin-associated glycoprotein (MAG) is minor myelin membrans proteins and may play a role in cell to cell interaction as a member of immunoglobulin superfamily. We completed cDNA cloning of mouse MAG and found two kinds of MAG isoforms (small-MAG : S-MAG, large-MAG : L-MAG) which are expressed by alter native splicing mechanism. To clarify one of mechanisms of regeneration in nervous system, we examined roles of MAG on remyelination after damage of nervous system. The results of this research program are as follows.
1) We established an experimental model of demyelination and remyelination by Cuprizon intoxication.
2) An model of secondary demyelination by occlusion of middle cerebral artery was established.
3) We prepared an anti-L-MAG and an anti-S-MAG antibodies from synthetic peptides of c-termini to L-MAG and S-MAG respectively.
4) The L-MAG isoform was induced during remyelinating stage after demyelination by Cuprison intoxication.
5) Changes of brain proteins including MAG were examined.
6) In the quaking mutant mouse, L-MAG was scarcely expressed throughout development.
Therefore, L-MAG is revealed to be important for normal myelination.
7) We have completed cDNA cloning of human MAG and obtained only L-MAG clone.
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