Comprehensive investigation of molecular mechansim of intracellular localization of DG kinase as an example of general enzmes
| Project/Area Number |
15K07002
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Functional biochemistry
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| Research Institution | Kobe University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TSURUTA HIROKI 神戸大学, 連携創造本部, 准教授 (20346282)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 脂質キナーゼ / ジアシルグリセロール / 可視化 / 結合タンパク質 / 細胞内局在変化 / チロシンリン酸化 / フォスファチジン酸 / 細胞周期 / 癌 / ホスファチジン酸 |
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| Outline of Final Research Achievements |
In this study, molecular mechanism of nuclear-cytoplasm shuttling of diacylglycerol kinase alpha (DGKa) was investigated. We found that RVH-EF region directly bound to C1 domain which functions as nuclear localization signal (NLS) nteraction was enhanced by tyrosin phosphorylation at Y218, resulting weaken the function of C1 domain as NLS. We also identified cyclin dependent kinase 12 and Rheb as binding proteins of DGKa in the nucleus and the cytoplasm, respectively. The former seems to work to stop the cell cycle and the latter seems to contribute the proliferation.
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Report
(3 results)
Research Products
(12 results)
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[Journal Article] A novel diacylglycerol kinase α-selective inhibitor, CU-3, induces cancer cell apoptosis and enhances immune response2015
Author(s)
1)Lui K, Kunii N, Sakuma M, Yamaki A, Mizuno S, Sato M, Sakai H, Kado S, Kumagai K, Kojima H, Okabe T, Nagano T, Shirai Y. and Sakane F
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Journal Title
J lipid res
Volume: ５７
Issue: 3
Pages: 368-379
DOI
Related Report
Peer Reviewed / Open Access
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