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. 2006 Mar;8(3):173–180. doi: 10.1593/neo.05625

Figure 4.

Figure 4

Effects of EBV latent infection on the NFκB pathway in nasopharyngeal epithelial cells. (A) EMSA showing the kinetics of NFκB binding activity in nuclear extracts isolated from EBV-infected and uninfected cells (left panel). The specificity of binding was determined by competition experiments in which a nuclear extract isolated from C666-1 cells was analyzed in the presence of a 50-fold excess of an unlabelled NFκB consensus probe or an NFκB mutant probe (right panel, lanes 1–4). The activation of p50-NFκB and p65-NFκB complexes was examined by supershift analysis using antibodies against p50 and p65. Antibody against STAT3 was used as negative control (right panel, lanes 5–8). (B) Western blot analysis of NFκB activity using antibody specific for the phosphorylated form of IκB. The total levels of IκB, p50-NFκB, and p60-NFκB were also examined. (C) Western blot analysis of NFκB downstream targets (VEGF and COX-2) associated with cell invasion, and of c-Myc and Bcl-xL in EBV-infected nasopharyngeal epithelial cells.