| Project/Area Number |
24592772
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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 |
Morphological basic dentistry
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| Research Institution | University of Miyazaki |
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Principal Investigator |
IGAWA Kaori 宮崎大学, 医学部, 助教 (90423722)
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| Co-Investigator(Kenkyū-buntansha) |
KANEDA Kazuko 大阪大学, 大学院医学系研究科, 特任助教 (00533209)
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| Co-Investigator(Renkei-kenkyūsha) |
MORISHITA Kazuhiro 宮崎大学, 医学部, 教授 (80260321)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 転写因子 / 骨分化 |
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| Outline of Final Research Achievements |
For investigation of Mel1/Prdm16 function, we produced the knock out mice, however we could establish only heterozygotic deficient lines, and homozygotic deficient mice became embryonic lethal. In other hands, facial malformation, cleft palate and abnormality incisor appeared in heterozygotic deficient mice. It suggested that Mel1/Prdm16 plays the important role in differentiation of bone differentiation. From the feature of deficient mice, it suggested that this gene is important in development of bone. Using osteoblast cell line and cartilage cell line, Mel1/Prdm16 works for the differentiation promoting in the cartilage cells, and suppressing in osteoblasts. In addition, Mel1/Prdm16 promote the nuclear translocation of the complex of R-Smad and Co-Smad in the cartilage cell line, and suppress that translocation to nuclear in osteoblasts. We are now analyzing of the mechanism of action of Mel1/Prdm16 in current bone differentiation.
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