| Project/Area Number |
25640065
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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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) |
UEDA Takeshi 広島大学, 原爆放射線医科学研究所, 助教 (60585149)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ヒストン脱メチル化 / Kdm2b / 白血病 / 造血幹細胞 / 酸化的リン酸化経路 / エネルギー代謝 / ヒストン脱メチル化酵素 / トランスジェニックマウス / 酸化的リン酸化 / Fbxl10 |
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| Outline of Final Research Achievements |
We found that overexpression of Kdm2b, a histone demethylase for histone H3K36, in hematopoietic stem cells induced leukemia and observed that genes involved in oxidative phosphorylation are activated in Kdm2b-overexpressing hematopoietic stem cells. In this study, we demonstrated that i) Kdm2b directly binds to several genes involved in oxidative phosphorylation and upregulates their expression patterns, ii) Kdm2b accelerates cell cycle of the S-phase but dose not affect cell cycle entry from G0 phase to G1 phase, and iii) Kdm2b enhances ATP production but dose not affect ROS production. These findings provide novel insights into the tumorigenic mechanisms by activation of oxidative phosphorylation from the viewpoint of energy metabolism.
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