| Project/Area Number |
21590072
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAGO Megumi 慶應義塾大学, 薬学部, 講師 (30445192)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 接着班キナーゼFAK / JAKキナーゼ / JAK2 V617F変異体 / Epoシグナル / STAT5の恒常的な活性化 / 腫瘍形成能 / リコカルコンA / JAK2点変異V617F / JAK2シグナル伝達 / STAT5 / c-Myc / GSK-3β / メラノーマ細胞 / 抗アポトーシス因子 / GSK-3βのリン酸化 / NF-κB阻害作用 / 接着分子FAK / JAK2 / チロシンリン酸化 / V617F変異体 / 真性赤血球増加症 |
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| Research Abstract |
(1) We previously reported that a FAKY929F mutant in the B16F10 melanoma cell line gave poor metastasis. Here, we identified that the phospholipid protein(PLP) 2 was downregulated in this cell line, acting as an effector molecule downstream of FAK. Why PLP2 induces the metastatic activity was investigated in vitro and in vivo.(2) A JAK2 mutant, JAK2V617F was constitutively active and induced abnormal proliferation, tumorigenesis in nude mice, as well as exhibited resistance to antitumor drugs including cisplatin. The reason why JAK2V617F has such potent activities was studied. We presented a notion that JAK2 mutation constitutively activated STAT5, which enhanced various transcription factors and kinases including c-Myc, Aurora kinaseA or Pim-1/2, thus inducing transformation in vitro and in vivo.
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