2017 Fiscal Year Final Research Report
Molecular differential inhibition mechanism of osteoclastic bone resorption by glucocorticoid-induced osteop orosis in childhood.
Project/Area Number |
26463115
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Orthodontics/Pediatric dentistry
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Research Institution | Kyushu Dental College |
Principal Investigator |
Maki Kenshi 九州歯科大学, 歯学部, 教授 (60209400)
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Co-Investigator(Kenkyū-buntansha) |
自見 英治郎 九州大学, 歯学研究院, 教授 (40276598)
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Project Period (FY) |
2014-04-01 – 2018-03-31
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Keywords | osteoclast / p130cas / Bif-1 / PCR / Osteoporosis |
Outline of Final Research Achievements |
Osteopetrosis due to dysfunction of osteoclasts in p130Cas-deficient mice suggest p130Cas play important roles for osteoclastic bone resorption. we focused Bif-1 which binding p130Cas because of the novelty, primary structure that can be involved in regulation of cytoskeleton. Western blotting and quantitative real-time PCR analysis showed the expression level of Bif-1 increased during osteoclastic differentiation. Bone mineral density of femurs isolated from Bif-1-deficient mice was higher than that of wild-type femurs using μCT analysis. These results suggest that Bif-1 is one of the candidate proteins to regulate osteoclastic bone resorption as a downstream molecule of p130Cas.
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Free Research Field |
小児歯科学会
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