| Project/Area Number |
24792289
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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 |
Orthodontic/Pediatric dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KAWAI Nobuhiko 徳島大学, ヘルスバイオサイエンス研究部, 助教 (40437588)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 骨格筋萎縮 / ユビキチンン-プロテアソーム経路 / IGF-1シグナル / ユビキチン-プロテアソーム経路 / Cbl-b / 機能性ペプチド |
|---|
| Research Abstract |
In atrophied muscles, ubiquitin ligase, Cbl-b, increases and it stimulates the ubiquitination and degradation of IRS-1, an intermediate in IGF-1 singnaling pathway, resulting in IGF-1 resistance. In this study, we evaluate the efficacy of application of anti-ubiquitination oligopeptide that inhibits the interaction between Cbl-b and IRS-1 into starved C2C12 myotubes and denervated tibialis anterior muscle of C57BL/6 wild-type mice. Oligopeptide significantly inhibited the decrease of AKT phosphorylation in starved myotubes. In addition, sectional area of denervated muscle fibers treated with oligopeptide was significantly larger compared to non-treated denervated muscles. These results suggest that application of anti-ubiquitination oligopeptide could be an effective tool for therapeutic use in muscular atrophy diseases.
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