| Project/Area Number |
23659153
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Kyoto University |
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Principal Investigator |
OKA Shogo 京都大学, 医学研究科, 教授 (60233300)
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| Co-Investigator(Renkei-kenkyūsha) |
KAWASAKI Nana 国立医薬品食品衛生研究所, 生物薬品部, 部長 (20186167)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 生体分子医学 / 機能糖鎖 / ジストログリカン / 硫酸基転移酵素 / 糖鎖 / 筋ジストロフィー / ラミニン |
|---|
| Research Abstract |
α-Dystroglycan undergoes extensive glycosylation required for the interaction between α-dystroglycan and the extracellular matrix such as laminin and aberrant glycosylation of α-DG has already been identified in the pathogenesis of several types of congenital muscular dystrophy. In this study, we revealed that a sulfotransferase, HNK-1ST, suppressed the glycosylation and reduced the ligand-binding activity of α-dystroglycan. We also found that HNK-1ST regulated the migration of melanoma cells through the glycosylation state on α-dystroglycan
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