| Project/Area Number |
23370086
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | Osaka University |
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Principal Investigator |
NOJIMA HIROSHI 大阪大学, 微生物病研究所, 教授 (30156195)
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| Co-Investigator(Renkei-kenkyūsha) |
YABUTA Norikazu 大阪大学, 微生物病研究所, 准教授 (10343245)
OKUZAKI Daisuke 大阪大学, 微生物病研究所, 助教 (00346131)
NAITO Yoko 大阪大学, 微生物病研究所, 特任研究員 (10553026)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥19,760,000 (Direct Cost: ¥15,200,000、Indirect Cost: ¥4,560,000)
Fiscal Year 2013: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2012: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2011: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | 染色体不安定性 / 中心体 / キナーゼ / M期チェックポイント / Lats / GAK / 細胞周期 / Cyclin G / リン酸化 / PP2A |
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| Research Abstract |
Tumor malignancy promotes cell invasion and metastasis, which is one of the factors that hamper effective cancer therapy. Tumor malignancy means that cancer cells frequently cause missegregation of chromosomes on every cell division to generate two daughter cells with distinct chromosome quantity; this cancer specific feature is called "chromosomal instability". In this study, we show that the centrosomal kinases, Lats1/2 and GAK, form three novel signaling pathways and regulate the stability of chromosomes: they are Aurora-A-Lats1/2-Aurora-B (ALB) and Chk1-Lats2-14-3-3-P-body (CLP) pathways for Lats1/2 and GAK-PP2A-B'gamma-Chk2/Condensin II (GBC) pathway for GAK. To realize efficient analysis, we generated knockout mice lacking Lats1, Lats2, GAK, Cyclin G1 and/or Cyclin G2 genes, and Lats2-defective cancer cells using TALEN/Crispr_Cas systems.
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