| Project/Area Number |
26860318
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | Tokyo Institute of Technology |
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Principal Investigator |
Isobe Tomoyasu 東京工業大学, 大学院生命理工学研究科, 科学研究費研究員 (40402341)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | エピジェネティクス / 慢性炎症 / 炎症 |
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| Outline of Final Research Achievements |
Chronic inflammation is known to be an important risk factor in cancer. Both global hypomethylation and site-specific hypermethylation in genomic DNA are observed in cancer, and it is believed that these abnormal DNA modifications disturb normal gene expression and affect genomic stability. Recently, we found that activation-induced cytidine deaminase (AID), which ectopically express in various inflammation-associated cancers including Helicobacter pylori-associated gastric cancer, activates methylated promoters and perturbs tumor-related gene expression (Isobe et al, 2013 FEBS Lett.), though the mechanisms which influence these modifications are yet to be defined. In this study, we performed shRNA library screening to reveal the mechanism by which AID induced DNA hypomethylation.
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