| Project/Area Number |
17014062
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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 | Kobe University |
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Principal Investigator |
MINAMI Yasuhiro Kobe University, 大学院・医学研究科, 教授 (70229772)
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| Co-Investigator(Kenkyū-buntansha) |
YODA AKINORI 神戸大学, 大学院・医学研究科, 助教 (70335454)
NISHITA MICHIRU 神戸大学, 大学院・医学研究科, 准教授 (30379359)
ENDO MITSUHARU 神戸大学, 大学院・医学研究科, 助教 (90436444)
YAMAGATA KAORU 神戸大学, 大学院・医学研究科, 助教 (80533786)
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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 |
¥69,900,000 (Direct Cost: ¥69,900,000)
Fiscal Year 2009: ¥13,900,000 (Direct Cost: ¥13,900,000)
Fiscal Year 2008: ¥13,900,000 (Direct Cost: ¥13,900,000)
Fiscal Year 2007: ¥13,900,000 (Direct Cost: ¥13,900,000)
Fiscal Year 2006: ¥13,900,000 (Direct Cost: ¥13,900,000)
Fiscal Year 2005: ¥14,300,000 (Direct Cost: ¥14,300,000)
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| Keywords | DNA損傷応答 / シグナル伝達 / がん化 / Chk2キナーゼ / Wip1ホスファターゼ / Wnt5a / Ror2シグナル / がんの浸潤 / 癌化 / 14-3-3 / 癌の浸潤 / がん原遺伝子産物 / がん抑制遺伝子産物 / チェックポイント機構 / リン酸化・脱リン酸化 / チェツクポイント機構 / チェックポイントキナーゼ / がん遺伝子産物 / 核内シングル伝達 / がんの分子標的治療 / DNA損傷 / Chk1キナーゼ / ATMキナーゼ / WIP1ホスファターゼ / 悪性腫瘍 |
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| Research Abstract |
It has been shown that following DNA damage anti-oncogenic protein kinases, including ATM, Chk1 and Chk2 kinases, are phosphorylated and activated, thereby executing checkpoint machinery, leading to cell-cycle arrest. Subsequently, oncogenic Wip1 phosphatase are induced by p53, and dephosphorylates and inactivates phosphorylated -protein kinases, thereby re-starts arrested cell-cycle. In addition, we have shown that in osteosarcoma cell lines constitutively active Wnt5a/Ror2 signaling induces matrix metalloproteinase-13, thereby confers invasive properties on osteosarcoma cells.
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