| Project/Area Number |
17012005
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TANIGUCHI Tadatsugu The University of Tokyo, 大学院・医学系研究科, 教授 (50133616)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAOKA Akinori 北海道大学, 遺伝子病制御研究所, 教授 (30323611)
TAMURA Tonohiko 東京大学, 大学院・医学系研究科, 准教授 (50285144)
HONDA Kenya 東京大学, 大学院・医学系研究科, 助手 (60334231)
OOBA Yuusuke 東京大学, 大学院・医学系研究科, 助手 (30333503)
YANAI Hideyuki 東京大学, 大学院・医学系研究科, 助教 (70431765)
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| Project Period (FY) |
2005 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥417,200,000 (Direct Cost: ¥417,200,000)
Fiscal Year 2009: ¥83,500,000 (Direct Cost: ¥83,500,000)
Fiscal Year 2008: ¥83,500,000 (Direct Cost: ¥83,500,000)
Fiscal Year 2007: ¥83,500,000 (Direct Cost: ¥83,500,000)
Fiscal Year 2006: ¥83,500,000 (Direct Cost: ¥83,500,000)
Fiscal Year 2005: ¥83,200,000 (Direct Cost: ¥83,200,000)
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| Keywords | インターフェロン / IRFファミリー / p53 / 樹状細胞 / 発がん抑制 / Noxa / Puma / Toll様受容体 / がん / 自然免疫 / IRF / 転写因子 / アポトーシス |
|---|
| Research Abstract |
We investigated biological mechanisms and role of effecter molecules, e.g. interferons, IRFs and Noxa. It revealed that these molecules are involved in transformation, apoptosis induction and metastasis signaling pathways. We also found the cross-talk pathway between TLRs signaling. Moreover, we identified DAI and HMGB1, 2, 3 are important for the nucleic-acid mediated innate immune responses. Since these pathways regulate tumorgenesis and exacerbation, our findings will be proved to be useful for the development of novel tumor therapy in near future.
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