| Project/Area Number |
24659910
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthodontic/Pediatric dentistry
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| Research Institution | Osaka University (2013-2014)
Okayama University (2012) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YANAGITA Takeshi 岡山大学, 大学病院, 助教 (90534793)
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | オートファジー / 骨代謝 / Atg5 / Twist2 / ATG5 / 遺伝子改変動物 / 部位特異的ノックアウトマウス |
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| Outline of Final Research Achievements |
Autophagy is a vesicle and lysosome-mediated catabolic mechanism that is essential for cell degradation of unnecessary or dysfunctional cellular components through the actions of lysosomes. This mechanism plays a wide variety of physiological and pathophysiological roles conserved. However, the physiological significance of autophagy has not yet been clarified in the process of bone metabolism. Conventional knockout of Atg5 alleles leads to lethal at or shortly after birth. In this study, we created a conditional knockout allele of the Twist2 (Dermo1) gene employing the Cre-loxP system. This promoter is active in the bone forming osteoblasts in skeletal development. From the gross appearance, Atg5 mutant did not show any significant differences in morphology. Micro CT analysis neither found bone phenotypes in the mutants. Although recent studies demonstrated that autophagy is involved in bone formation, bone specific Atg5 deficiency did not demonstrated bone phenotypes.
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