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| Reference : Role of the Protein Kinase C Lambda/Iota Isoform in Nuclear Factor-Kappab Activation by ... |
| Scientific journals : Article | |||
| Life sciences : Biochemistry, biophysics & molecular biology | |||
| http://hdl.handle.net/2268/18501 | |||
| Role of the Protein Kinase C Lambda/Iota Isoform in Nuclear Factor-Kappab Activation by Interleukin-1beta or Tumor Necrosis Factor-Alpha: Cell Type Specificities | |
| English | |
| Bonizzi, G. [> > > >] | |
Piette, Jacques  [Université de Liège - ULg > Département des sciences de la vie > Virologie - Immunologie >] | |
| Haterte, Stéphanie [Université de Liège - ULg > Département des sciences de la santé publique > Informatique médicale et biostatistique >] | |
| Merville, Marie-Paule [Université de Liège - ULg > Département de pharmacie > Chimie médicale >] | |
| Bours, Vincent [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Génétique générale et humaine] | |
| 15-Mar-1999 | |
| Biochemical Pharmacology | |
| 57 | |
| 6 | |
| 713-20 | |
| Yes (verified by ORBi) | |
| International | |
| 0006-2952 | |
| [en] It has previously been reported that distinct signaling pathways can lead to nuclear factor (NF)-kappaB activation following stimulation of different cell types with inflammatory cytokines. As the role of atypical protein kinase C (PKC) isoforms in NF-kappaB activation remains a matter of controversy, we investigated whether this role might be cell type-dependent. Immunoblots detected atypical PKC expression in all the analyzed cell lines. The PKC inhibitor calphostin C inhibited NF-kappaB activation by tumor necrosis factor (TNF)-alpha or interleukin (IL)-1beta in Jurkat or NIH3T3 cells but not in MCF7 A/Z cells. Cell transfections with a PKC lambda/iota dominant negative mutant abolished TNF-alpha-induced NF-kappaB-dependent transcription in NIH3T3 and Jurkat cells but not in MCF7 A/Z cells. Similarly, the same mutant blocked NF-kappaB-dependent transactivation after IL-1beta stimulation of NIH3T3 cells, but was ineffective after IL-1beta treatment of MCF7 A/Z cells. In MCF7 A/Z cells, however, the PKC lambda/iota dominant negative mutant could abolish transactivation of an AP-1-dependent reporter plasmid after stimulation with TNF-alpha but not with IL-1beta. These data thus confirm that transduction pathways for NF-kappaB activation after cell stimulation with TNF-alpha or IL-1beta are cell-type specific and that atypical PKC isoforms participate in this pathway in NIH3T3 and Jurkat cells. | |
| http://hdl.handle.net/2268/18501 |
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