2015 Fiscal Year Final Research Report
Exploring the inflammation-autoimmune-fibrosis interaction by using novel mouse model for fibrosis and scleroderma
Project/Area Number |
25461497
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Collagenous pathology/Allergology
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Research Institution | Kyoto University |
Principal Investigator |
Ashida Noboru 京都大学, 医学(系)研究科(研究院), 講師 (00538978)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | 線維化 / 炎症 / 強皮症 / 自己免疫 |
Outline of Final Research Achievements |
To explore the role of NFκB in fibrosis, we made mice with deletion of IKKβ, an essential kinase for the activation of NFκB, in myofibroblasts. The mice presented massive fibrosis in skin and internal organs more in females, and autoantibodies were detected in serum. We submitted world patent application claiming this mouse as a novel animal model for fibrosis and scleroderma. We tried to unveil the mechanism of this phenotype, and found that kinase-independent function of IKKβ is responsible for the phenotypes, and identified AMAP1 as a binding protein with IKKβ.
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Free Research Field |
循環器内科学、分子生物学
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