Fig. 4: TRAF5 and RIPK1 have no major effect on death receptor-induced IL-8 induction.
From: TRAF2 and RIPK1 redundantly mediate classical NFκB signaling by TNFR1 and CD95-type death receptors
A Expression of TRAF2 and TRAF5 in HCT116-PIK3CAmut, HCT116-PIK3CAmut-TRAF5, HCT116-PIK3CAmut-TRAF2KO and HCT116-PIK3CAmut-TRAF2KO-TRAF5 cells. B IL-8 secretion after overnight stimulation with TNF (100 ng/ml) or Fc-CD95L (200 ng/ml) of cell line variants shown in A. Data shown are mean +/− SEM of six independent experiments. IL-8 production was statistically evaluated in similarly treated pairs of cells transfected or not with TRAF5 by t-test. ***p < 0.001. C The indicated HCT116-PIK3CAmut variants were stimulated with 100 ng/ml TNF and total cell lysates were analyzed by western blotting with respect to the indicated protein species. One of two experiments with similar result is shown. D RIPK1-deficient variants of HCT116-PIK3CAmut, HeLa-RIPK3 and HT29 cells along with their parental counterparts were analyzed for DR-induced IL-8 production as described in B, n = 6. IL-8 production was statistically evaluated by one-way ANOVA (Bonferroni post-hoc test) *p < 0.05, **p < 0.01. ***p < 0.001. E Western blot analysis of phosphorylation and degradation of IκBα upon stimulation with TNF (100 ng/ml). One of two experiments with similar result is shown.
