| Project/Area Number |
21591320
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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 |
Pediatrics
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| Research Institution | Osaka University |
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Principal Investigator |
|
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| Co-Investigator(Renkei-kenkyūsha) |
MOHRI Ikuko 大阪大学, 連合小児発達学研究科, 准教授 (70399351)
|
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| Research Collaborator |
ABE Sanae 大阪大学, 歯学研究科, 大学院生
FUJIWARA Makoto 大阪大学, 医学系研究科, 大学院生 (50625697)
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| Project Period (FY) |
2009 – 2011
|
| 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 | 甲状腺ホルモントランスポーター / 軟骨細胞 / 成長軟骨 / 成長障害 / 乏突起膠細胞 / トランスレーショナルリサーチ / Allan-Herndon-Dudley症候群 / MCT8 / MCT10 |
|---|
| Research Abstract |
The Allan-Herndon-Dudley syndrome(AHDS), caused by monocarboxylate transporter 8(MCT8) mutations, is characterized by severe psychomotor retardation. We focused on two symptoms, delayed myelination and relatively normal growth compared to patients with congenital hypothyroidism and demonstrated that# 1) oligodendrocyte precursor cells express MCT8 and# 2) Monocarboxylate transporter 10(MCT10) plays a role in growth plate chondrocyte proliferation and differentiation
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