| Project/Area Number |
23657086
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional biochemistry
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| Research Institution | Tokyo Institute of Technology |
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Principal Investigator |
DENDA kimitoshi 東京工業大学, 生命理工学研究科, 助教 (50212064)
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| Co-Investigator(Kenkyū-buntansha) |
KOMADA Masayuki 東京工業大学, 大学院・大学院・生命理工学研究科, 教授 (10225568)
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| Project Period (FY) |
2011 – 2012
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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 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Ser/Thrキナーゼ / ノックアウトマウス / 胎盤 / 分娩 / X染色体不活化 / Ser/Thr キナーゼ / 分娩異常 / 遺伝子欠損マウス |
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| Research Abstract |
Nrk(NIK-related kinase) is a functionally unknown Ser/Thr protein kinase. To elucidate the physiological roles of Nrk, we generated a strain of mice with targeted disruption of the Nrk gene in the X chromosome. The Nrk gene knockout causes overgrowth of the placenta, indicating that Nrk is a key regulator of placental cellular proliferation. In addition, when the Nrk-null fetuses were dominant, the pregnant dam failed to deliver offspring at term. Thus, Nrk appears to be important for performing parturition.
In order to investigate the molecular mechanisms leading to the Nrk knockout phenotype, protein expression levels in the Nrk knockout placenta were compared with those in wild type tissues by using high-performance two-dimensional electrophoresis methodology, and found several significant protein spots whose expression levels were enhanced or diminished significantly in the Nrk knockout placenta. Our examine whether placentas or fetus are essential for labor is now in progress.
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