Fig. 2: TRAF2 is largely dispensable for death receptor-induced NFκB-mediated IL-8 production.
From: TRAF2 and RIPK1 redundantly mediate classical NFκB signaling by TNFR1 and CD95-type death receptors
A Cells were stimulated as indicated with 100 ng/ml TNF, 200 ng/ml Fc-CD95L, 200 ng/ml TRAIL, 20 µM ZVAD or 90 µM necrostatin-1 (Nec-1). After 16–18 h, IL-8 production was quantified by ELISA analysis of cell culture supernatants. Shown are the mean +/− SEM of 4 independent experiments. IL-8 production was statistically evaluated by two-way ANOVA of parental and TRAF2-deficient cells. ***p < 0.001; **p < 0.01; *p < 0.05. B Cells were treated as indicated with 100 ng/ml TNF, 200 ng/ml Fc-CD95L, 20 µM TPCA-1 or 20 µM MLN4924. After 16–18 h, IL-8 production was quantified by ELISA analysis of cell culture supernatants. Shown are the mean +/− SEM of 4 independent experiments. IL-8 production data sets of untreated, TPCA-1 and MLN4923 were statistically evaluated by one-way ANOVA (Bonferroni post-hoc test). ***p < 0.001; **p < 0.01; *p < 0.05.
