2012 Fiscal Year Final Research Report
Analysis of acute myeloid leukemia development mechanisms induced by MOZ/MLL fusion genes
| Project/Area Number |
23791094
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Hematology
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| Research Institution | National Cancer Center Japan |
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Principal Investigator |
KATSUMOTO Takuo 独立行政法人国立がん研究センター, 研究所, 研究員 (50469970)
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| Project Period (FY) |
2011 – 2012
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| Keywords | 発現制御 / 癌 / 幹細胞 / 発生・分化 |
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| Research Abstract |
In this study, I mainly analyzed roles of endogenous MOZ in leukemogenesis induced by MOZ/MLL fusion genes. As a result, I revealed that endogenous MOZ was essential for maintenance of active histone marks in target gene loci induced by MOZ/MLL fusion genes. Endogenous MOZ was also critical for suppression of INK4A tumor suppressor gene. These results suggest that endogenous MOZ was critical for leukemogenesis to maintain chrom
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[Journal Article] The Hbo1-Brd1/Brpf2 complex is responsible for global acetylation of H3K14 and required for fetal liver erythropoiesis.2011
Author(s)
Yuta Mishima, Satoru Miyagi, Atsunori Saraya, Masamitsu Negishi, Mitsuhiro Endoh, Takaho A. Endo, Tetsuro Toyoda, Jun Shinga, Takuo Katsumoto, Tetsuhiro Chiba, Naoto Yamaguchi, Issay Kitabayashi, Haruhiko Koseki, Atsushi Iwama
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Journal Title
Blood
Volume: 118
Pages: 2443-53
Peer Reviewed
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