| Project/Area Number |
23590153
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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 |
Environmental pharmacy
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| Research Institution | Hoshi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IMAI Masahiko 星薬科大学, 医薬品化学研究所, 助教 (40507670)
TAKAHASHI Noriko 星薬科大学, 医薬品化学研究所, 教授 (50277696)
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| Co-Investigator(Renkei-kenkyūsha) |
AMANO Hitoshi 昭和大学, 歯学部, 准教授 (90212571)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 脂溶性ビタミン / 骨代謝 / 胎盤 / 細胞周期 / アミノ酸トランスポーター / ｐ５７Ｋｉｐ２ / 骨芽細胞 / 核内受容体 / p57Kip2 / 脂溶性生理活性物質 / ビタミンＡ / ビタミンＤ / 長鎖不飽和脂肪酸 |
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| Research Abstract |
A CDK inhibitor, p57Kip2, might be one of the molecules for osteogenesis, because p57-ablated mice displayed delay of bone formation. So, we assumed that p57 could regulate the bioactivities of the certain vitamins or hormones for bone formation. Here we have found out that p57 bound VDR, vitamine D3 receptor, and was necessary for VDR's activity, which is the transcription factor. And p57 KO mice also displayed placentamegaly with trophoblastic displasia.
p57 affected on the expression levels and cellular localization of ASCT2, which acts for the cell fusion in trophoblast-differentiation. Now we are examining the mechanism of the p57's activity on ASCT2 on placentamegaly.
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