| Project/Area Number |
22770118
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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 |
Functional biochemistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
SUIDU Futoshi 北海道大学, 遺伝子病制御研究所, 講師 (90431379)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | タンパク分解 / リン酸化 / AKT / ユビキチン / セリンスレオニンキナーゼ / ダウン症 / 21Trisomy / TTC3 / タンパク質分解 / Akt / 21トリソミー / ２１トリソミー |
|---|
| Research Abstract |
In order to elucidate the biological function of TTC3, which we previously identified as a novel ubiquitin ligase of Akt kinase, we analyzed an effect of ectopic expression of TTC3 into HEK 293T cells. Overexpression of TTC3 into 293T cells resulted in reduction of cell growth rate. Conversely, induction of siRNA of TTC3 into HT1080 caused acceleration of cell growth, meaning that TTC3 function as negative regulator of cell growth by inhibiting of Akt activity. By using 21 trisomy Down syndrome-derived cell lines, which TTC3 protein is spontaneously overexpressed, TTC3 knock down by siRNA induced enhancement of Akt activity. Collectively, TTC3 may function as a cell growth regulatorby modulating PI3K-Akt pathway in mammalian cells.
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