| Project/Area Number |
24659668
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
HONMA Masashi 東京大学, 医学部附属病院, 助教 (60401072)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 骨代謝 / 骨形成 / 骨吸収 / シグナル伝達 / 薬理活性 / 生体分子 / 生理活性 / 薬理学 / 老化 |
|---|
| Research Abstract |
RANKL is known as a signal input molecule which stimulates mature osteoclast formation, and anti-RANKL neutralizing antibody can suppress osteoclast formation in vivo. By contrast, we have shown that osteoblastic RANKL acts as a signal accepting molecule for osteclast-derived RANK and up-regulates bone formation. Based on these results, we hypothesized that a properly designed macromolecule, which binds RANKL extracellular domain, can stimulate bone formation and inhibit bone resorption simultaneously. We screened human single chain Fv library and finally obtained a clone which stimulates bone formation and suppress bone resorption simultaneously as a trimer.
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