| Project/Area Number |
18591074
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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 | Kumamoto University |
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Principal Investigator |
OKADA Seiji Kumamoto University, Center for AIDS Research Division of Hematopoiesis, Professor (50282455)
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| Co-Investigator(Kenkyū-buntansha) |
SUZU Shinya Kumamoto University, Center for AIDS Research Division of Hematopoiesis, Associate Professor (80363513)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,880,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥480,000)
Fiscal Year 2007: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | BCL6 / AP-1 / c-Fos / Hematopoietic cells / Erythroblast / Dendritic cells / B cells / 造血幹細胞 |
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| Research Abstract |
The proto-oncogene bcl-6 and c-fos are ubiquitously expressed in various tissues, and play important role for the differentiation, proliferation, apoptosis and oncogeneisis. In this study, I focused on the function of bcl-6 and c-fos for the hematologic cells, using transgenic and gene deficient mice.
1. Function of Bcl-6 on erythroid differentiation
Bcl-6 detected in the TER119highCD7lhigh subset of erythroblasts in the spleen of neonatal mice may be required to retain the erythroblasts in the cell proliferation stage. In addition, we found that ABCG-2 is also expressed in erythroblast of all of the maturation stage.
2. Function of Bcl-6 on dendritic cell differentiation
Bcl-6 deficient mice showed decreased umber of dendritic cells in spleen. Especially CD8+ subfraction of dendriti cells was completely deficient,.
3. Function ofBCL6 on B cell differentiation
We have found that ADAR1 (RNA-editing adenosine deaminase) is one of the target gene of BCL6, and loss of Bc16 cause the higher frequency of somatic hypermultation on B cells.
4. Effect of c-Fos ro the regulation of TCRβ recombination.
We have found that c-fos directly promotes RAG1/2 binding to the RSS and regulate TCRβ recombination ordering and allelic exclusion.
5. Analysis of hematopoietic niche in c-Fos deficient mice.
We have found that Magakaryocyte-like cells are appeared in the spleen of c-Fos deficient mice and play an important role in the hematopoietic niche.
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