Figure 4. Positive feedback control of JNK1 phosphorylation by NF-κB through DUSP1. A: Time-dependent increases in p- IκBα. Scrambled shRNA subline was exposed to CAP (20 µM) for up to 90 min. Western blots reveal the time course of changes in p-IκBα formation, which serves as a readout of NF-κB activation. B: Contribution by JNK1 to IκBα phosphorylation. Western blots compare CAP (20 µM)-induced IκBα phosphorylation in scrambled shRNA and JNK1 sublines at 60 min. Preincubation with either 5z-OX (0.1 µM), CPZ (10 µM) or PDTC (50 µM) for 60 min suppressed CAP-induced IκBα phosphorylation. C: Positive feedback control by NF-κB of JNK1/2 activation. Loss of NF-κB activation reduces transient JNK1/2, p38, and ERK1/2 MAPK activation induced by CAP (20 µM) for up to 90 min. Summary plots contrast time-dependent patterns of MAPK activation in the scrambled shRNA subline (left) with those in NF-κB1 subline (right). D: Inverse relationship between changes in PKCδ and DUSP1 expression. Scrambled shRNA and NF-κB1 sublines were exposed to CAP (20 µM) as described in B. Summary plot (left) indicates that in the scrambled shRNA subline CAP-induced increases in PKCδ expression whereas DUSP1 remained invariant (left). Summary plot (right) reveals inverse responses by PKCδ and DUSP1 to CAP in NF-κB1 subline.