Regulation of oncogenic activities by TRB1 through TGF-beta signaling
Project/Area Number |
26860042
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Biological pharmacy
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Research Institution | Nagoya City University |
Principal Investigator |
Itoh Yuka 名古屋市立大学, 薬学研究科(研究院), 助教 (40454326)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | TGF-β / TRB1 / がん / シグナル伝達 / TGFβ / TRBファミリータンパク質 |
Outline of Final Research Achievements |
TRB1 is a mammalian ortholog of Tribbles in drosophila. TRB1 has a conserved substrate-binding domain of a protein kinase, but not ATP-binding and kinase-activation domains, as well as other TRB family proteins (TRB2 and TRB3). While some reports including our study have suggested that TRB1 plays important roles on cancer progression, the function of TRB1 has not been fully elucidated. In this study, we found that TRB1 represses TGF-β signaling by inhibiting interaction between Smad and DNA and expression of TRB1 protein is induced by TGF-β in a manner dependent of Smad activation.
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Report
(3 results)
Research Products
(19 results)