Figure 4

A putative model for Nrf2-–Nfkb1 interactions in inflammation and carcinogenesis. Chemical signals generated by dietary chemopreventive agents or toxicants, or inflammatory signals, may cause Nrf2 nuclear translocation that sets in motion a dynamic machinery of coactivators and corepressors that may form a multimolecular complex with Nrf2 for modulating transcriptional response through the antioxidant response element, ARE. Inflammation may also cause release of NF-κB from IκB and stimulate NF-κB nuclear translocation to modulate transcriptional response through the NF-κB response element, NF-κB-RE, along with the cofactors of NF-κB. Several members of the MAPK family may act in concert with Nrf2 and Nfkb1 with multiple interactions between the members of the putative complex to elicit the chemopreventive and pharmacotoxicological events in inflammation and carcinogenesis.