| Project/Area Number |
15K14378
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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 |
Tumor biology
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| Research Institution | Tokyo Institute of Technology |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KOMADA Masayuki 東京工業大学, 科学技術創成研究院, 教授 (10225568)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | プロテインキナーゼ / 胎盤 / 乳腺 / がん / 周産期 / 遺伝子欠損マウス / 細胞増殖制御 / セリンスレオニンプロテインキナーゼ / ノックアウトマウス |
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| Outline of Final Research Achievements |
Breast cancer is the most common malignant tumor among Japanese women. However, its pathogenesis is still unclear, and the prevalence of breast cancer has a major impact on health worldwide.
We have searched for the physiological roles of NRK, a novel X chromosome-linked Ser/Thr protein kinase which belongs to the germinal center kinase family. In this research, we demonstrated one of the female-specific critical role for NRK through generation and phenotypic analysis of mice deficient for the protein kinase gene. The mammary gland is an branched ductal tree that completes the majority of its development in the postnatal mammalian following puberty, and continues to undergo constant remodeling during reproductive cycles and functional differentiation during pregnancy. We provide evidence that NRK is involved in suppressing the pathologial development of breast tumor associated with the mammary gland hyperplasia during pregnancy by phenotype analysis of the Nrk-knockout mutant mice.
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