| Project/Area Number |
24650610
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Carcinogenesis
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| Research Institution | Tokyo Institute of Technology |
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Principal Investigator |
KOMADA Masayuki 東京工業大学, 生命理工学研究科, 准教授 (10225568)
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| Co-Investigator(Kenkyū-buntansha) |
DENDA Kimitoshi 東京工業大学, 大学院生命理工学研究科, 助教 (50212064)
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 癌 / 細胞・組織 / シグナル伝達 / 蛋白質 / 酵素 / 細胞増殖 / 胎盤 / 乳腺 / 腫瘍 / タンパク質 |
|---|
| Research Abstract |
1) We identified CSIG (cellular senescence-inhibited gene), a protein which inhibits PTEN in the Akt signal transduction pathway, as a Nrk-binding protein in placenta, suggesting that Nrk inhibits the proliferation of spongiotrophoblasts in placenta by inhibiting the Akt signaling pathway. We also found that the level of a cell cycle inhibitor protein p27 is downregulated in Nrk knockout spongiotrophoblasts, suggesting that Nrk increases p27 gene expression or inhibits p27 protein degradation in spongiotrophoblasts.
2) We found that the estrogen level is elevated in the blood and ovary of mammary tumor-harboring Nrk knockout female mice, suggesting that the high estrogen level in the blood causes mammary tumors in Nrk knockout mice. In addition, we found that Nrk is expressed in lactating and old (~12 months) wild-type mice, suggesting that Nrk suppresses the overgrowth of mammary epithelial cells by downregulating estrogen synthesis in the ovary.
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