2005 Fiscal Year Final Research Report Summary
The study of the molecular mechanism underlying leukemogenesis caused by the translocation involving a novel polycomb-group gene, ASXH2
| Project/Area Number |
16590956
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
KAKAZU Naoki Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Department of Molecular-Targeting Cancer Prevention, Research Associate, 医学研究科, 助手 (20264757)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Leukemia / ASXH2 / 2p23 translocation |
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| Research Abstract |
In a previous study, in a pediatric therapy-related myelodysplastic syndrome (tMDS) with t(2;8)(p23;p11), the reciprocal transcript of MOZ-ASXH2 was not detected. The MOZ-ASXH2 chimeric transcript was only isolated from the breakpoints suggests that the MOZ-ASXH2 transcript, and not the ASXH2-MOZ, seem to play an important role in leukemogenesis. The predicted MOZ-ASXH2 fusion protein consists of 2228 amino acids and contains 809 amino acids derived from MOZ. The moiety of MOZ retains the PHD-type zinc finger, the MYST domain displaying HAT activity, and a small part of the acidic region of MOZ. Almost all part of the ASXH2 protein, omitting the amino terminal 19 amino acids, is combined to it. This structural feature is very similar to those of the other MOZ fusions, MOZ-CBP, MOZ-p300, and MOZ-TIF2, being pathogenic to AML-M4 or M5 type. This supports the idea that MOZ-ASXH2 is leukemogenic fusion protein.
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