| Project/Area Number |
25430075
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
Masaki Toshihiro 帝京科学大学, 医療科学部, 教授 (00585028)
Hagiwara Hiroki 帝京科学大学, 医療科学部, 教授 (80276732)
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| Co-Investigator(Renkei-kenkyūsha) |
Saito Fumiaki 帝京大学, 医学部, 准教授 (40286993)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ジストログリカン / 糖鎖修飾 / 蛋白質プロセッシング / トランスジェニックマウス / 神経系 |
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| Outline of Final Research Achievements |
The N-terminal domain of α-dystroglycan (α-DG-N) is cleaved and secreted from many types of cells. However, the functional role of secreted α-DG-N is still unidentified. To elucidate this point, we generated transgenic mice overexpressing α-DG-N ubiquitously. Interestingly, we demonstrated that the reactivity of IIH6, an antibody which detects specific sugar chain structure of α-dystroglycan, was markedly reduced in skeletal muscle. In contrast, laminin binding activity was well preserved. Based on these results, we propose that the evaluation not only of IIH6 reactivity but also of the laminin binding activity is necessary for the clinical diagnosis of α-dystroglycanopathies.
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