2017 Fiscal Year Final Research Report
The role of Zip10 during skeletogenesis
| Project/Area Number |
15K11050
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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 |
Functional basic dentistry
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| Research Institution | Showa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
FUKADA Toshiyuki 徳島文理大学, 薬学部, 教授 (70373363)
IRIE Tarou 岩手医科大学, 歯学部, 教授 (00317570)
MISHIMA Kenji 昭和大学, 歯学部, 教授 (50275343)
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| Research Collaborator |
IWAMOTO Motomi メリーランド大学, 整形外科, 准教授
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 軟骨 / 骨格形成 / 細胞・組織 / 遺伝子 |
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| Outline of Final Research Achievements |
Zinc deficiency during development causes severe skeletal defects including deformity and a decrease in bone mass. However, the underlying molecular mechanisms have remained unclear. The aim of this study is to investigate the role of zinc transporter ZIP10, an SLC39 family member during skeletogenesis. We generated bone- and cartilage-specific ZIP10 conditional knockout (Zip10-cKO) mice using Cre/loxP system. Zip10-cKO embryos (E16.5-17.5) showed dwarfisms with short limbs, narrow chest space, and deformation of calvaria with decreasing calcification. These results suggest that ZIP10 is essential for skeletogenesis during embryonic development and that ZIP10 plays important roles in the regulation of cell viability/survival and substance transport in skeletal cells, likely via zinc homeostasis.
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| Free Research Field |
細胞分子機能病理学
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