| Project/Area Number |
16616002
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
アレルギー
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| Research Institution | Chiba University |
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Principal Investigator |
KASUYA Yoshitoshi Chiba University, Graduate School of Medicine, Associate Professor, 大学院・医学研究院, 助教授 (70221877)
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| Co-Investigator(Kenkyū-buntansha) |
SUDO Tatsuhiko RIKEN, Antibiotics Laboratory, 抗生物質研究室, 研究員 (30260227)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | p38 / knock-out mice / transgenic mice / bleomycin / Interstitial lung disease / p38MAPキナーゼ / アレルギー / 成因分子機構 |
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| Research Abstract |
We conducted the following two research projects.
I)To elucidate the new molecular mechanism of allergic skin disease, a direct interaction between p38 MAPK and FK506-binding protein (FKBP) was investigated. However, the regulation of p38 MAPK by the direct interaction with FKBP was not confirmed. In the process of this project, we successfully identified three new spliced transcripts of FKBP-12 and investigated their tissue-specific expression (submitted to Gene).
II)To elucidate the molecular mechanism for allergic lung disease, p38α-KO mice and transgenic mice in which p38 dominant-negative form is expressed in a lung-specific manner (p38d.n.-TG) were subjected to bleomycin administration. Bleomycin, anti-cancer drug is known to induce interstitial lung disease as a side effect. We investigated a static compliance of the lung from wild, p38α-KO and p38d.n.-TG mice two weeks after l, t, bleomycin administration. The static compliance of the lung from bleomycin-administered wild mice was significantly decreased compared that from saline-administered wild mice. In contrast, the bleomycin-induced decrease in static lung compliance was not observed in case of p38α-KO and p38d.n-TG, suggesting that p38α is involved in bleomycin-induced interstitial lung disease. We are further investigating this point.
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