| Project/Area Number |
23791215
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatrics
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| Research Institution | Institute for Developmental Research, Aichi Human Service Center |
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Principal Investigator |
NISHIZAKI Yuriko 愛知県心身障害者コロニー発達障害研究所, 周生期学部, リサーチレジデント (90378901)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | SIP1 / 神経管閉鎖 / 二分脊椎症 / Sip1 / BMP / Wnt-PCPパスウェー / 細胞極性 |
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| Research Abstract |
The aim of this study is to elucidate the mechanism of neural tube closure defects. For this purpose, we analyze the SIP1 knock-out mice as a spina bifida model. The apical localization of several molecules participating neural tube contraction were found to be insufficient. The phosphorylation of Smad5 on the dorsal side of the neural tube of the SIP1 knock-out embryo was not observed. A part of the neural ectoderm cells of the SIP1 knock-out embryo abnormally differentiated and transformed into the epithelial-like cells with a bleb morphology. These results give some insights into the unknown function of SIP1 in neural tube closure, a fundamental biological process harboring etiologies of spina bifida.
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