| Project/Area Number |
23590566
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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 |
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| Co-Investigator(Kenkyū-buntansha) |
HIDA Shigeaki 信州大学, 医学系研究科, 准教授 (10345762)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ASC / Inflammasome / innate immunity / cell death / cancer / fascin / IL-1beta / IFNbeta / Inflamasome / inflammasome / 細胞死 / がん / 炎症 / 分子相互作用 / 細胞増殖制御 / 免疫監視機構 |
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| Research Abstract |
ASC responsible for inflammasome fomrmation is involved in both pro-inflammation and pro-apoptosis. We observed the occurrence of the colon cancer was clearly retarded by ASC deletion from Ahr-/-mouse, a prone to colon cancer. In Ahr-/-mice, it was observed that an oncogene beta-catenin was accumulated in nuclei of the intestinal epithelium associated with an increase in the epression of IL-1 1 beta and severe inflammation was suppressed. On one hand, we observed that the metastatic potential of cancer cells were enhanced by ASC knock-down, while Asc over-expression suppressed the survival of cancer cells specifically in the confluent state.
When we searched for the ASC binding proteins by immunoprecipitaiton and mass spectrometer, cytoskeletal and signal transduction-relating molecules, such as Fascine and IQGAP were, and their direct interaction with ASC was confirmed. The investigation of the biological significance of the interaction is underway.
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