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- W1974555221 abstract "Cytokine-stimulated IκBα degradation is impaired in HT-29 and primary intestinal epithelial cells. To gain more insight into the mechanism of this defect, we dissected cytokine-induced NF-κB signaling pathway in HT-29 cells. IL-1β and TNF, alone or in combination with IFNγ, failed to induce IκBα or IκBβ degradation in HT-29 cells. Despite similar 125I-IL-1β binding, HT-29 cells displayed no IRAK degradation, a 75% reduction of IKK activity, and decreased IκBα phosphorylation, NF-κB DNA binding activity and IL-8 mRNA accumulation in response to IL-1β compared to Caco-2 cells. Selective activation of NF-κB pathway by adenoviral delivery of NF-κB-inducing kinase (Ad5NIK) or IKKβ (Ad5IKKβ) strongly activated IKK activity (>20 fold) in HT-29 cells with concomitant endogenous IκBα serine 32 phosphorylation and total IκBα degradation. In addition, NF-κB DNA binding activity and IL-8 secretion is higher in Ad5NIK-infected than in IL-1β-stimulated HT-29 cells. These data show that altered NF-κB signaling is associated with impaired stimulation of an upstream IKK activator." @default.
- W1974555221 created "2016-06-24" @default.
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- W1974555221 date "2004-06-01" @default.
- W1974555221 modified "2023-10-15" @default.
- W1974555221 title "NF-κB-inducing kinase restores defective IκB kinase activity and NF-κB signaling in intestinal epithelial cells" @default.
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- W1974555221 doi "https://doi.org/10.1016/j.cellsig.2003.11.007" @default.
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