Mechanisms of assembly and inhibition of DNA replication factors including MCM proteins
| Project/Area Number |
26440002
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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 |
Molecular biology
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| Research Institution | Ibaraki University |
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Principal Investigator |
Ishimi Yukio 茨城大学, 理学部, 教授 (80159772)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | MCMヘリカーゼ活性 / DNA複製フォーク / タンパク質相互作用 / MCM2-7複合体 / DNAヘリカーゼ / DNA複製制御 / CDKによるリン酸化 / MCM4変異 / 細胞がん化 / MCM4/6/7複合体 / HIF-１A / MCM2-7機能発現制御 / 細胞周期 / ヘリカーゼ / タンパク質リン酸化 / タンパク質集合 |
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| Outline of Final Research Achievements |
Following three points should be stressed as novel findings. As to the effects of MCM4 mutations on MCM2-7 complex formation, mutations from cancer cells affect MCM complex formation through changes in interaction with other MCM members. Furthermore, it is suggested that the presence of the mutant MCM4 affects DNA replication in HeLa cells. It has been shown that a number of MCM-interacting proteins bind to conserved MCM-box, suggesting that these proteins regulate MCM function through the activity. The amino-terminal region of MCM4 is shown to be required for DNA helicase activity of MCM4/6/7 complex. It is suggested that the phosphorylation of the region with CDK can destabilize MCM complex.
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Report
(4 results)
Research Products
(7 results)
