| Project/Area Number |
23390252
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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 |
Hematology
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| Research Institution | Hiroshima University |
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Principal Investigator |
HONDA Hiroaki 広島大学, 原爆放射線医科学研究所, 教授 (40245064)
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| Co-Investigator(Kenkyū-buntansha) |
INABA Toshiya 広島大学, 原爆放射線医科学研究所, 教授 (60281292)
UEDA Takeshi 広島大学, 原爆放射線医科学研究所, 助教 (60585149)
HONDA Zen-ichiro お茶の水女子大学, 保健管理センター, 教授 (70238814)
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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 |
¥19,240,000 (Direct Cost: ¥14,800,000、Indirect Cost: ¥4,440,000)
Fiscal Year 2013: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2012: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2011: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
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| Keywords | ヒストン脱メチル化酵素 / Fbxl10 / トランスジェニックマウス / 白血病 / 造血幹細胞 / Fbx110 |
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| Research Abstract |
We generated transgenic mice that overexpress Fbxl10, a histone demethylase, in hematopoietic stem cells (HSCs), and found that the mice develop leukemia at about 1 year after birth. By bone marrow transplantation, we demonstrated that the leukemia was caused by enhanced HSC-intrinsic proliferative potentials. In addition, we found that neuron specific gene 2 (Nsg2), which encodes a protein involved in intracellular transport, was overexpressed and that genes involved in oxidative phosphorylation in mitochondria were significantly up-regulated. Our findings provide novel insights in the leukemogenic mechanisms from the viewpoint of energy metabolism and intracellular transport.
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