Mechanism of conversion of TGF-beta from tumor suppressor to malignant factor by post-translational modification control
| Project/Area Number |
15K07936
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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 |
Biological pharmacy
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| Research Institution | Nagoya City University |
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Principal Investigator |
Inoue Yasumichi 名古屋市立大学, 大学院薬学研究科, 准教授 (10450579)
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| Co-Investigator(Renkei-kenkyūsha) |
HAYASHI HIDETOSHI 名古屋市立大学, 大学院薬学研究科, 教授 (80198853)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
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: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | TGF-beta / Smad / p53 / 翻訳後修飾 / TGF-β / ユビキチン化 / 脱ユビキチン化酵素 / シグナル伝達 / Smad2/3 / アセチル化 / エピジェネティクス / SET8 / ヒストンメチル化 |
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| Outline of Final Research Achievements |
It is known that TGF-beta is involved in carcinogenesis as a growth factor, but also has the effect of promoting malignancy of cancer. However, how these contradictory physiological effects are controlled remains unclear. In this study, we found that methyltransferase SET8 is one Smad cofactor that mediates its action. It also revealed that the tumor suppressor gene p53 is a cofactor that follows up the cancer suppressive action of TGF-beta.
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Report
(4 results)
Research Products
(56 results)
