| Project/Area Number |
25640063
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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 | Kobe University |
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Principal Investigator |
Kamada Shinji 神戸大学, バイオシグナル総合研究センター, 教授 (20243214)
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| Co-Investigator(Renkei-kenkyūsha) |
KIKKAWA Ushio 神戸大学, バイオシグナル総合研究センター, 教授 (40150354)
NAKASHIMA Akio 神戸大学, バイオシグナル総合研究センター, 准教授 (70397818)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 細胞老化 / DNA損傷 / p53 / 活性酸素 / アミノ酸代謝 |
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| Outline of Final Research Achievements |
To understand the molecular mechanisms of cellular senescence when DNA damages occurred, we identified and characterized several genes that are crucial for senescence. By using a developed experimental system in which cellular senescence or apoptosis is induced preferentially by altering the concentration of etoposide, a DNA-damaging drug to induce DNA double-strand brakes, we compared gene expression profiles of senescent and apoptotic cells by microarray analysis and identified several genes specifically upregulated in senescent cells. Among these genes, we focused on proline dehydrogenase and D-amino acid oxidase. It was clarified that both genes played crucial roles in senescence by producing reactive oxygen species as byproducts in amino acid metabolism.
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