Genetic analysis of defense response against intracellular infection, induced by environmental stress response pathway.
| Project/Area Number |
21780045
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Applied entomology
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| Research Institution | Iwate Medical University |
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Principal Investigator |
TERASHIMA Jun Iwate Medical University, 薬学部, 助教 (60400272)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | 昆虫分子生物学 / 感染防御 |
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| Research Abstract |
Ecdysone inducible protein 75B (E75B) is one of the ecdysone response genes and relates to metamorphosis in the insects. E75B has a role for nutritional shortage response, regulates the development of ovary in Drosophila under nutritional stress. Ecdysone is the insect steroid hormone and adjusts not only the metamorphosis but also stress response in Drosophila. We expected that steroid relate pathway has possibility to response against various stress in not only the insect but also mammalian cell, tried to apply the microarray analysis data to the investigation of stress response in human cancer, a human liver carcinoma cell line (HepG2). In this project, we show that E75B has important role for defense response against obligate intracellular parasite, Nosema bombycis in Drosophila melanogaster and low-glucose conditions induce the translocation of AhR into the nucleus in the human carcinoma cell line HepG2 and that AhR activates CYP1A1, CYP1A2, and CYP1B1 expression. The activation of CYP1 family member expression indicates that AhR binds to a ligand and successfully functions as a transcription factor. These results suggest that an endogenous AhR ligand is produced in HepG2 cells under low-glucose conditions and that AhR's role as a transcription factor is related to the low-glucose response of HepG2 cells.
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Report
(3 results)
Research Products
(11 results)
