| Project/Area Number |
25650031
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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(Renkei-kenkyūsha) |
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) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Ser/Thrキナーゼ / 胎盤 / 妊娠 / 分娩不全 / 遺伝子ノックアウト / Ser/Thr キナーゼ / 遺伝子ノックアウトマウス / X染色体不活化 / 分娩異常 / セリン／トレオニンキナーゼ / 遺伝子欠損マウス |
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| Outline of Final Research Achievements |
Nrk (Nik-related kinase) encoded in the X chromosome is a physiologically mysterious Ser/Thr protein kinase, which belongs to the germinal center kinase family. On a whole-body level in mice, disruption of the nrk gene resulted in the placental overgrowth, suggesting that Nrk acts as a regulator of cell proliferation in the organ. It has also observed that the nrk-null fetuses influence the pregnant dam to be delay of labor.
To shed light on the molecular mechanisms lying behind the nrk-null phenotyes, we isolated a series of Nrk-binding proteins by using two-hybrid analysis and co-immunoprecipitation. In addition, proteomics analysis against the nrk gene distrupted placenta were performed using the high performance two-dimentional polyacrylamide gel electrophoresis. We identified several proteins whose expression levels were varied significantly. Our research how Nrk acts as a device for controlling labor induction will clarify the complexities in the process of pregnancy and labor.
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