| Project/Area Number |
12671864
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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 |
Conservative dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
YAMAZAKI Muneyoshi Nihon University, School of Dentistry at Matsudo, Professor, 松戸歯学部, 教授 (30050032)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | Human mafB / Leucine zipper (bZIP) / Quantitative RT-PCR / monocyte / T-cell / h-mafB / 定量的RT-PCR法 / T-ヘルパー細胞 / maf B / ロイシンジッパー / モノサイト |
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| Research Abstract |
We have studied the expression of a human homologue of mafB (maf-1), a member of the family of large maf transcription factors. The exact boundaries of the homodimerization domain of mafB were characterized by the yeast 2-hybrid system and found to be confined to the leucine zipper domain. Real-time quantitative RT-PCR method was applied to study the tissue distribution of mafB expression in several human cell lines. In support of the suggested key role that mafB expression plays in differentiating macrophages, we found mafB to be expressed at a very high level in monocytic U937 and THP-1 cell lines. However, we show here that mafB transcription is not restricted to myeloid cells but can also be detected in lymphoid cells indicating transcriptional plasticity during hematopoiesis. Activation of T cells in the presence of growth factor IL-2 and IL-4 or IL-12 downregulates the MafB transcript level. In conclusion, strong proliferative signals mediated by T cell activation and interleukines (IL-4 and IL-12) alter the MafB mRNA level when resting naive CD4^+ T helper cells enter the differentiation pathway in vitro.
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