Skip to main content
. Author manuscript; available in PMC: 2017 Jun 6.
Published in final edited form as: Sci Signal. 2016 Dec 6;9(457):ra120. doi: 10.1126/scisignal.aaf1129

Fig. 7. The role of the RelA:p52–induced, late-phase synthesis of IκBα in costimulated macrophages in insulating canonical and noncanonical NF-κB signalingpathways.

Fig. 7

TLR4 stimulation induces the nuclear activity of the RelA:p50 dimer, which is subjected to rapid negative feedback by IκBα. Costimulation through LTβR generates a late RelA:p52–containing NF-κB activity in fibroblasts. In costimulated macrophages, however, the RelA:p52 dimer triggersed the hyperactive Nfkbia promoter, which leads to the production of IκBα additionally at late time points. This late-phase IκBα synthesis attenuatesd the late-acting RelA:p50 and RelA:p52 activities in costimulated macrophages and abrogatesd crosstalk between the canonical and noncanonical NF-κB pathways. Early and late signaling events have been indicated with solid and dashed lines, respectively.