| Project/Area Number |
13670328
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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 |
Immunology
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| Research Institution | Chiba Cancer Center Research Institute |
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Principal Investigator |
OH Keiyou Chiba Cancer Center Research Institute, Division of Pathology, Research Fellow, 病理研究部, 研究員 (80231041)
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| Co-Investigator(Kenkyū-buntansha) |
TAGAWA Masatoshi Chiba Cancer Center Research Institute Division of Pathology Head, 病理研究部, 部長 (20171572)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | lymphocyte / proliferation / gene expression / immune response / transcription factor / CD40 / B cell antigen receptor / 免疫学 / 遺伝子 / アポトーシス / シグナル伝達 |
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| Research Abstract |
To explore the molecular events that drive a resting B cell to enter the cell cycle, we have employed a modified subtractive cloning strategy to identify novel genes whose expression is regulated upon B cell activation through CD40, which interacts with CD40 ligand transiently expressed by activated T cells. In the past two years, we focused on the function in vivo of Clast1 and Clast5 genes. B cells from Clast1 tratnsgenic mice are hyper-reactive to antigen receptor signaling. In addition, both primary and secondary immune responses to T-dependent antigens are enhanced. These preliminary findings strongly suggest a role for Clast1 in augmenting B cell responses. In Clast5 transgenic mice, the size and cell number of both spleen and thymus are greatly reduced. Moreover, B cell responses to a variety of stimuli are impaired. Progenitor B cells in the bone marrow have a significantly reduced growth response to IL-7. These results indicate that Clast5 is a negative regulator of B cell activation and may serve to determine the threshold of B cell responses. We are in the process of generating Clast1 and Clast5 knock out mice.
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