| Project/Area Number |
21591099
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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 |
Neurology
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SAITO Fumiaki 帝京大学, 医学部, 講師 (40286993)
HAGIWARA Hiroki 帝京大学, 医学部, 客員准教授 (80276732)
SHIMIZU Teruo 帝京大学, 医療技術学部, 教授 (00107666)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 神経分子病態学 / 筋ジストロフィー / ジストログリカン / ラミニン / LARGE / 糖鎖修飾 / 分子標的治療 / 福山型先天性筋ジストロフィー / 脳神経疾患 / 翻訳後修飾 / 糖転移酵素 / 糖鎖 / Large |
|---|
| Research Abstract |
We generated transgenic mice overexpressing a glycosyltransferase, LARGE. The mice were born and grew normally, and laminin binding activity of dystroglycan was greatly increased in the skeletal muscle. We crossed the transgenic mice with dy^<2J> mice, a mouse model of congenital muscular dystrophy, to examin therapeutic effect of LARGE overexpression. The dystrophic change of dy^<2J> mice overexpressing LARGE, however, was not improved and the degeneration of myofibers was rather deteriorated.
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