Project/Area Number |
23616009
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
epigenetics
|
Research Institution | National Hospital Organization, Kyushu Cancer Center |
Principal Investigator |
ODA Hisanobu 独立行政法人国立病院機構(九州がんセンター臨床研究センター), その他部局等, その他 (30295133)
|
Co-Investigator(Kenkyū-buntansha) |
NAKABEPPU Yusaku 九州大学, 生体防御医学研究所, 教授 (30180350)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | エピジェネティクス / 染色体 / ヒストン修飾 / ヒストンメチル化酵素 / H4リジン20 / 細胞周期 / DNA複製 / クロマチン / PR-Set7 / ヒストン / メチル化 / ヒストンメチル化 / ヒストンメチルトランスフェラーゼ / set8 / 遺伝子ノックアウトマウス |
Research Abstract |
Histone post-translational modifications impact many aspects of chromatin and nuclear function. Histone H4 Lysine 20 methylation (H4K20me) has been implicated in regulating diverse processes ranging from the DNA damage response, chromatin condensation, and DNA replication to gene regulation. PR-Set7 is the sole enzyme that catalyzes monomethylation of H4K20. It is required for maintenance of all levels of H4K20me, and, importantly, loss of PR-Set7 is catastrophic for the various stages of development such as embryonic development and skin differentiation. These findings have placed PR-Set7, H4K20me, and proteins that recognize this modification as central nodes of many important pathways. The results were published in two journals, Genes & Development and EMBO Journal.
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