Studies on stimulus-specific induction of a novel NF-κB regulator, IκB-ζ, and its physiological roles
Project/Area Number |
17590252
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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 |
General medical chemistry
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Research Institution | KYUSHU UNIVERCITY |
Principal Investigator |
TAKESHIGE Koichiro Kyushu University, Graduate School of Medical Sciences, Professor, 医学研究院, 教授 (10037450)
|
Co-Investigator(Kenkyū-buntansha) |
YAMAZAKI Soh Kyushu University, Graduate School of Medical Sciences, Assistant Professor, 医学研究院, 講師 (70315084)
牟田 達史 九州大学, 医学研究院, 助教授 (60222337)
大場 誠介 九州大学, 医学研究院, 特任助手 (80380666)
|
Project Period (FY) |
2005 – 2006
|
Project Status |
Completed (Fiscal Year 2006)
|
Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
Keywords | Innate Immunity / IκB-ζ / Regulation of Transcription / mRNA Stabilization / Signaling |
Research Abstract |
IκB-ζ is barely detectable in resting macrophages and is strongly induced upon stimulation with lipolysaccharide(LPS) or Interleukin (IL)-1β but not tumor necrosis factor(TNF)-α. The induced IκB-ζ associates with the NF-κB submit in the nucleus and regulates its transcriptional activity both positively and negatively depending on promoter structures of genes. In the present study, we investigated mechanisms that determine the different functions of IκB-ζ and found that IκB-ζ acts as an essential transcriptional activation by forming a complex with NF-κB on promoters harboring the NF-κB and C/EBP binding sites, upon stimulation of Toll-Like receptors or IL-1 receptor. We also analyzed the molecular mechanisms for the differential induction of IκB-ζ and found that the stability of IκB-ζ mRNA is specifically upregulated by stimulation with LPS or IL-1β but not TNF- α and that a 165-bp fragment present in the 3'-UTR of IκB-ζ mRNA confers the stimulus-specific induction and is essential for the induction of IκB-ζ.
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Report
(3 results)
Research Products
(16 results)