Analysis of tumor suppressors RASSF3 and RASSF6
Project/Area Number |
26460359
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General medical chemistry
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Research Institution | Tokyo Medical and Dental University |
Principal Investigator |
Iwasa Hiroaki 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (70582188)
|
Co-Investigator(Renkei-kenkyūsha) |
Maruyama Junichi 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (30723639)
|
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: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | シグナル伝達 / 腫瘍抑制 / フェイルセーフ / RASSF / 翻訳後修飾 |
Outline of Final Research Achievements |
Ras association domain family (RASSF) cooperates with tumor suppressors. The RASSF tumor suppressor genes are frequently inactivated in many types of human cancer. In this study we found that a novel tumor suppressor acts through RASSF. We also found that a cellular precursor state of tumor changes the structure of RASS protein to suppress tumor formation. Thus we propose that RASSF is a primary fail-safe mechanism of oncogene-driven tumorigenesis.
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Report
(4 results)
Research Products
(7 results)
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[Journal Article] A cell-based screening for TAZ activators identifies ethacridine, a widely used antiseptic and abortifacient, as a compound that promotes dephosphorylation of TAZ and inhibits adipogenesis in C3H10T1/2 cells.2015
Author(s)
Kawano S, Maruyama J, Nagashima S, Inami K, Qiu W, Iwasa H, Nakagawa K, Ishigami-Yuasa M, Kagechika H, Nishina H, Hata Y.
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Journal Title
J. Biochem.
Volume: 158
Issue: 5
Pages: 413-423
DOI
NAID
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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