| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Research Abstract |
It has been proposed that the metastasis suppressor CD82 regulates biological activity by associating with cell surface receptors or proteins. We reported previously that the CD82-c-Met complex inhibits hepatocyte growth factor (HGF)-induced cancer cell migration by the inactivation of small GTP-binding proteinsof the Rho family via c-Met adapter proteins. On the other hand, β-catenin binds tothe cytoplasmic domain of E-cadherin and links E-cadherin to the actin cytoskeleton through α-actinin, forming strong intercellular junction. In addition, the function of E-cadherin is regulated by binding p120 to the cytoplasmic domain of E-cadherin.E-cadherin has been implicated not only in cell adhesion but also in the signaling of cell migration. Our results suggested that CD82 regulated the signaling ofE-cadherin-catenin-actinin-actin cell cytoskeleton and inhibited cell migration withsupporting cell adhesion.
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