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. 2018 May 1;10(5):129. doi: 10.3390/cancers10050129

Figure 3.

Figure 3

Site-directed mutagenesis of the putative TLR2 binding motif in the EBV-dUTPase inhibits NF-κB activation. TLR2-HEK293 cells were transiently transfected with NF-κB luciferase reporter plasmid as we have described [40,43,44]. After 24–36 h, cells were treated with wild-type EBV-dUTPase, a triple mutant (82ELR84 to 82GGG84) of the EBV-dUTPase TLR2 putative binding motif (EBVdUTPase/TMutTLR2BD), EBV-dUTPase peptide L83-K103, scrambled peptide L83-K103 (10 μg/mL) or left untreated for 8 h and luciferase reporter gene activity was measured. Values represent the mean fold induction (FI) ± SD relative to control (n = 3). * p < 0.05 (Groups compared: dUTPase treated vs. untreated and dUTPase triple mutant vs. wild-type dUTPase).