2015 Fiscal Year Final Research Report
Inflammation control by novel nuclear IkB, IkBL
| Project/Area Number |
25460503
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Tokai University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 自己免疫 / 炎症 / NFkB |
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| Outline of Final Research Achievements |
Contribution to the inflammation control by I kappa B-like (IkBL) was examined. Tg mice showed reduced severity of experimentally-induced arthritis, mainly resulting from reduced function of innate immune cells such as macrophages. However, KO mice did not show significant change in the severity of acute inflammation induced by cecal ligation and puncture (CLP) or LPS injection. It is found that IkBL showed inhibitory effect on the transactivation of NFkB dependently on its nuclear translocation and that IkBL binds specifically to RelB protein, suggesting that it is involved in the control of inflammation through the modification of RelB function. Physiological significance of IkBL is to be further investigated.
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| Free Research Field |
免疫学 細胞生物学
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