| Project/Area Number |
26460376
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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 |
General medical chemistry
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
多胡 憲治 自治医科大学, 医学部, 講師 (20306111)
太田 聡 自治医科大学, 医学部, 講師 (40528428)
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| 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: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ST2 / LPS / シグナル伝達 / 細胞がん化 / LPS受容体 / 細胞形質転換 / 炎症反応 / TLR4 / MD2 / IL-33 / CD14 |
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| Outline of Final Research Achievements |
We investigated the mechanism of inhibitory effect of soluble ST2 protein, which is the extracellular domain of IL-33 receptor (ST2L protein), against the LPS signal transduction. ST2 protein did not inhibit the binding of LPS with LPS receptor. Each component of LPS receptor complex, TLR 4, CD14 and MD2, did not show the binding with ST2 protein, and each combination of two components of above also failed to bind with ST2, which suggests higher structure of LPS receptor complex is required for the binding with ST2.
Furthermore, We found novel proteins such as IFITM3 which bind with ST2L protein, and IL-33 is indispensable for the cellular transformation by Ras independent of ST2 protein, and IL-33 promotes the translation of cyclin D.
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