| Project/Area Number |
20591129
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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 |
Hematology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
OOTSUYAMA Kenichirou Yamaguchi University, 大学院・医学系研究科, 助教 (10432741)
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| Co-Investigator(Kenkyū-buntansha) |
KAWANO Michio 山口大学, 大学院・医学系研究科, 教授 (40161343)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Keywords | PPAR / NF-kB / 多発性骨髄腫 / CD54 |
|---|
| Research Abstract |
I indicated that PPARβ could suppress constitutive nuclear factor -κB (NF-κB) activity by PPARβ directly interacted with NF-κB. NF-κB is a dimeric transcription factor that can be formed by the assembly of five diverse proteins, p50, p52, Re1A (p65), Re1B and c-Re1 which, in combination, specify the dimer trancriptional activity. Although there were activated NF-κB in nucleus, in primaly myeloma cells, all NF-κB family was identified in the nucleuses. The PPARβ agonist carbacyclin induced multiple myeloma cell apoptosis. After stimulation of carbacyclin, PPARβ translocated to the nucleus. NF-κB-DNA- binding activity was also decreased in the nucleus of myeloma cell lines. And it was identified PPARβ associated with NF-κB (Re1A/ p65) . These results suggested that PPARβ activation could prevent nucler translocation of NF-κB and decrease the activity of NF-κB binding the promoter of NF-κB target genes in myeloma cell lines.
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