MAP3K regulation of immune cell development and function
Project/Area Number |
20590496
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Immunology
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Research Institution | The Institute of Physical and Chemical Research |
Principal Investigator |
SHINOHARA Hisaaki The Institute of Physical and Chemical Research, 分化制御研究グループ, 研究員 (10391971)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
Keywords | NF-kappaB / MAP3K / シグナル伝達 / NF-κB / 獲得免疫 / 抗原受容体 |
Research Abstract |
MAP3K, TAK1 is shared in adaptive and innate immune signaling. We generated and analyzed B cell conditional deletion of TAK1 using mb1-cre. In periphery, TAK1-deficient B cells showed impaired activation of NF-kB, proliferation, survival, and diffrentiation induced by anti-IgM. TAK-deficient bone marrow B cell also showed significant decreased differentiation in some subsets. Thus these analysis suggest TAK1 is essential for B cell differentiation.
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Report
(4 results)
Research Products
(12 results)
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[Journal Article] Dephosphorylation of Carma1 by PP2A negatively regulates T cell activation2011
Author(s)
Eitelhuber A C., Warth S., Schimmack G., Duwel M., Hadian K., Demski K., Beisker W., Shinohara H., Kurosaki T., Heissmeyer V., Krappmann D.
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Journal Title
EMBO J 30(3)
Pages: 594-605
Related Report
Peer Reviewed
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