| Project/Area Number |
24590578
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Shinshu University |
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Principal Investigator |
TAKI Shinsuke 信州大学, 学術研究院医学系, 教授 (50262027)
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| Co-Investigator(Renkei-kenkyūsha) |
HIDA Shigeaki 信州大学, 学術研究院医学系, 准教授 (10345762)
SANJO Hideki 信州大学, 学術研究院医学系, 助教 (50391967)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | サイトカイン / 好塩基球 / サイトカインレセプター / 細胞内シグナル伝達 / シグナル伝達 |
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| Outline of Final Research Achievements |
Structure-function relationship in the beta-c subunit of the IL-3 receptor for the intracellular signals for IL-4 production was investigated. In the past, technical limitations made studies of the beta-c cytoplasmic structure confined to those for survival/growth signals. We here developed a new experimental system that enabled us to examine the roles of beta-c substructures for IL-4 production as well as for survival/growth in primary murine basophils. As previously shown, beta-c lacking the entire cytoplasmic region or the so-called box1 region, to which Jak2 kinase bound, failed to transduce IL-3 signals for survival/growth and IL-4 production. In contrast, beta-c mutants lacking the more distal box2 region or with Phe-to-Tyr substitution at position 573 could support basophil survival/growth normally but were inefficient in triggering IL-4 production. This study is the first to identify unique beta-c subregions important for the IL-3 signals for effector functions.
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