| Project/Area Number |
25860858
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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 | Osaka University |
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Principal Investigator |
Kubota Takuo 大阪大学, 医学(系)研究科(研究院), 助教 (40629135)
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| Research Collaborator |
Fujiwara Makoto 大阪大学, 歯学部附属病院, 助教 (50625697)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 小児科学 / 骨代謝学 / 骨粗鬆症 / スクレロスチン / くる病 / 線維芽細胞 / 骨細胞 / 転写因子 / 骨石灰化 / Wntシグナル |
|---|
| Outline of Final Research Achievements |
Sclerostin, encoded by SOST, is a secretory protein that suppresses osteogenesis by inhibiting Wnt signaling. However, the regulatory mechanism underlying SOST expression remains unclear. We identified four transcription factors, ATF3, KLF4, PAX4, and SP7 that induced SOST expression and sclerostin secretion in human dermal fibroblasts. Parathyroid hormone suppressed the induced SOST and sclerostin, whereas hypoxia and prostaglandin E2 increased the induced SOST. This model may contribute to elucidating the regulatory mechanisms underlying SOST expression and advancing drug development for metabolic bone diseases.
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