| Project/Area Number |
21790320
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Osaka University (2010)
Hiroshima University (2009) |
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Principal Investigator |
YAMAMOTO Hideki Osaka University, 医学系研究科, 准教授 (20372691)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 分子病態学 / Wnt / Wntシグナル / Wnt5a / Wnt11 / Frizzled / エンドサイトーシス / クラスリン / Rac / Dkk1 / Frizzled受容体 / LRP6受容体 |
|---|
| Research Abstract |
We examined whether the internalization of Wnt receptors affects the ability of Dkk1 and Wnt5a to regulate Wnt signaling pathways. A secreted protein Dkk1, which acts as an inhibitor of Wnt signaling, reduced the amount of LRP6 from the lipid raft and induced clathrin-mediated internalization of LRP6 to suppress β-catenin pathway. Wnt5a activated Rac in the β-catenin-independent pathway, and Frizzled 2 (Fz2), clathrin, arrestin, and Ror1 or Ror2 were required for this action. These results indicate that Wnt signaling pathway is regulated by the internalization of Wnt receptors.
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