The elucidation of the mechanism of novel insulin signal via TRIM/RBCC E3 ligase
| Project/Area Number |
25870908
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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 |
General medical chemistry
General physiology
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| Research Institution | Kanagawa Institute of Technology |
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Principal Investigator |
Inoue Hideki 神奈川工科大学, 応用バイオ科学部, 准教授 (20550156)
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| Co-Investigator(Renkei-kenkyūsha) |
HORI TOSHIYUKI 立命館大学, 生命科学部, 教授 (70243102)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | インスリンシグナル / 寿命制御 / ユビキチン / シグナル伝達 / ユビキチン化 |
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| Outline of Final Research Achievements |
The forkhead transcription factor, DAF-16/FOXO, is a central regulator of the insulin signaling. DAF-16/FOXO proteins are indispensable for many cellular and biological processes such as lifespan regulation, proliferation and homeostasis. However, the entire molecular mechanisms involved in regulating DAF-16/FOXO transcriptional activation remain undefined. We found that NHL-1/TRIM3, TRIM/RBCC E3 ligase, positively regulates DAF-16/FOXO activity via stabilizing these proteins. NHL-1 positively regulates longevity, whereas TRIM3 increases oxidative stress resistance and suppresses cell proliferation. Moreover, we found some regulators including E1 and E2 enzymes by yeast two hybrid screening. These results delineate that the conserved NHL-1/TRIM3 regulates insulin/IGF signaling.
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Report
(4 results)
Research Products
(3 results)
