Molecular mechanism of non-genomic action of ecdysone
Project/Area Number |
21380035
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Applied entomology
|
Research Institution | Kanazawa University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
IWAMI Masafumi 金沢大学, 自然システム学系, 教授 (40193768)
|
Co-Investigator(Renkei-kenkyūsha) |
FUJIMOTO Yoshinori 東京工業大学, 理工学研究科, 教授 (50173472)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥18,460,000 (Direct Cost: ¥14,200,000、Indirect Cost: ¥4,260,000)
Fiscal Year 2011: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2010: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2009: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
|
Keywords | エクジソン / カイコガ / 絹糸腺 / 細胞死 / グルコース / オキシダーゼ / 膜受容体 / 前部絹糸腺 / 幼若ホルモン / 抑制因子 |
Research Abstract |
Although it is generally accepted thatecdysoneexerts itseffects through binding with nuclear ecdysone receptor, other receptor on plasma membrane acts as a ecdysone receptor(mEcR) that mediates ecdysone action without gene expression(non-genomic action). mEcR is suggested pharmacologically to be G protein-coupled receptor(GPCR). The activated GPCR activates the signal transduction pathway, which culminates caspase 3-like protease activation and induces cell death. In addition, we showed that ecdysone action against cell death was regulated non-endocrinologically. Anterior silk glands contain glucose oxidase that mediates production of hydrogen peroxide(H_2O_2), and H_2O_2suppresses the ecdysone action, i. e., progression of cell death.
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Report
(4 results)
Research Products
(21 results)