Fig 7. TTSS-mediated NF-κB activation is not dependent on TRAF6 or RIP2.

(A) TRAF6^-/- or RIP2^-/- or wt HEK293 cells were transfected with the NF-κB reporter plasmid and infected with W3110 strains, as indicated. NF-κB activation was determined by the dual luciferase assay. Two independent clones of TRAF6^-/- and RIP2^-/- were tested. (B) TRAF6^-/- mouse embryonic fibroblasts were treated with IL-1β, or infected with different EPEC strains, as indicated. The cells were then fixed, stained for p65 and quantified for nuclear p65 by microscopy. (C) HEK393 cells co-transfected with the NF-κB reporter plasmid and a plasmid expressing dominant negative RIP2 (DN-RIP2) were treated with MDP, tri-DAP, or infected with EPEC or W3110 strains, as indicated. NF-κB activation was determined by the luciferase assay.