| Project/Area Number |
24659467
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Shinichiro 慶應義塾大学, 医学部, 教授 (50160718)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 5q-症候群 / 骨髄異形成症候群 / ATOX1 / 造血幹細胞 / 血球分化 / 5q- 症候群 |
|---|
| Research Abstract |
5q- syndrome is a subtype of myelodysplastic syndrome characterized by a deletion of chromosome 5q33. To elucidate molecular pathogenesis of 5q- syndrome, we focused on ATOX1, a cupper chaperone located in the common deleted region of 5q33. Frequencies of hematopoietic stem cells (HSCs), multipotent hematopoietic progenitors, and lineage-committed progenitors in the bone marrow were normal in ATOX1-/- mice, and ATOX1-/- HSCs maintained normal self-renewal and long-term repopulating capacities. These results suggest that ATOX1 is not essential for HSC function and hematopoietic differentiation, and that ATOX1 has little, if any, roles in 5q- syndrome.
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