Fig. 3.

YopJ modifies IKKα and IKKβ. (a) Various proinflammatory stimuli activate the NF-κB-signaling pathway by activating the IκB kinase (IKK) complex. IKK activation results in the phosphorylation and subsequent ubiquitin-mediated degradation of IκB, the inhibitor or NF-κB. The removal of IκB results in NF-κB translocation to the nucleus where it can regulate gene expression. (b) HEK293 cells transfected with YopJ-wt or YopJ-C172A were stimulated with TNF-α. IκB degradation is slowed down (Top) by the expression of YopJ-wt (but not the C172A inactive mutant of YopJ). This effect is due to reduced phosphorylation of IκB in these cells (Middle) caused by inhibition of activation of IKK (Bottom) caused by WT YopJ. (c and d) Overexpression of IKKα (c) or IKKβ (d) results in their activation in cells expressing inactive YopJ-C172A but this activation is blocked by WT YopJ (Upper). Total levels of IKKα and IKKβ are not affected by expression of YopJ (Lower).