Reference : Interleukin-1 Beta Induces Nuclear Factor Kappa B in Epithelial Cells Independently o...
Scientific journals : Article
Human health sciences : Oncology
http://hdl.handle.net/2268/2312
Interleukin-1 Beta Induces Nuclear Factor Kappa B in Epithelial Cells Independently of the Production of Reactive Oxygen Intermediates
English
Bonizzi, Giuseppina [> > > >]
Dejardin, Emmanuel mailto [Université de Liège - ULg > > Virologie - Immunologie >]
Piret, Bernard [> > > >]
Piette, Jacques mailto [Université de Liège - ULg > Département des sciences de la vie > Virologie - Immunologie >]
Merville, Marie-Paule mailto [Université de Liège - ULg > Département de pharmacie > Chimie médicale >]
Bours, Vincent mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Génétique générale et humaine]
15-Dec-1996
European Journal of Biochemistry
242
3
544-9
Yes (verified by ORBi)
International
0014-2956
[en] A large body of work has been devoted to tumor necrosis factor alpha or interleukin-1 beta (IL-1 beta) signaling leading to the activation of the transcription factor nuclear factor-kappa B (NF-kappa B) in various cell types. Several studies have indicated that NF-kappa B activation depends strictly on the production of reactive oxygen intermediates. In this report, we first demonstrated that IL-1 beta is a potent activator of NF-kappa B in various epithelial transformed cell lines (OVCAR-3, SKOV-3, MCF7 A/Z). In these cells, IL-1 beta rapidly induces NF-kappa B through a complete degradation of I kappa B-alpha, while H2O2 activates NF-kappa B with slower kinetics through a partial degradation of I kappa B-alpha, p100 and p105. We showed that IL-1 beta-mediated induction of NF-kappa B in OVCAR-3 and in other epithelial cell lines does not proceed through the production of reactive oxygen intermediates, while the same cytokine activates NF-kappa B in lymphoid cells through the intracellular generation of H2O2. Our study demonstrated that several signaling pathways lead to the activation of NF-kappa B, following IL-1 beta treatment in different cell types.
http://hdl.handle.net/2268/2312

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