| Project/Area Number |
17591544
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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 |
Orthopaedic surgery
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
HIRANO Fuminori Asahikawa Medical College, Medicine, Lecturer, 医学部, 講師 (60250552)
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| Co-Investigator(Kenkyū-buntansha) |
FUKAWA Etsushi Asahikawa Medical College, Medicine, Assistant Prof., 医学部, 助手 (60322913)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | signal transduction / immunology / nucleic acids / clinical research / gene regulation |
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| Research Abstract |
We have studied that effect of NF-κB regulation in rheumatoid arthritis synovitis under controlling IκBβ2 expression in order to diminish the inflammation of synovitis. NF-κB is a transcription factor and plays a pivotal role in regulating synovitis in rheumatoid arthritis. In unstimulated cells, NF-κB binds to inhibitory molecules IκBs and exists in cytoplasm. Especially, IκBβ2 has the strongest inhibitory effect against NF-κB activation in IκBs. However, little is known about IκBβ2 expression and regulation in synovial cells with rheumatoid arthritis. First, we showed that IκBβ2 expression was significantly decreased in rheumatoid arthritis synovial cells as compared with in normal or osteoarthritis synovial cells. Moreover, when IκBβ2 was strongly expressed in synovial cells using expression plasmids, NF-κB activation was clearly repressed. Next, we have examined the half-life of IκBβ2 using 3'-untranslated lesion of IκBβ2-fused luciferase-gene expression plasmid. IκBβ2 half-life was shortening in rheumatoid arthritis synovial cells as compared with in normal or osteoarthritis synovial cells. In addition, we presented that several RNA binding proteins bound to 3'-untranslated lesion of IκBβ2 and those proteins were decreased or deleted in rheumatoid arthritis synovial cells. Collecting those results, the synovitis in rheumatoid arthritis was more strongly inflamed due to the decrease of IκBβ2 expression. We now investigate to clone new RNA binding proteins and to exam the function of those proteins.
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