Signaling Pathways, Chemical and Biological Modulators of Nucleotide Excision Repair: The Faithful Shield against UV Genotoxicity

Figure 7

Modulation of the NFE2L2 pathway in fibroblasts. The NFE2L2 pathway in fibroblasts can be either activated or inhibited depending on the administered compound. ROS, eotaxin, and curcumin mediate the release of NFE2L2 from the inhibitor KEAP1. Flavone via the activation of MAPK1 facilitates the phosphorylation of NFE2L2. In addition, Mrp1 removes glutathione conjugates to drugs in a NFE2L2-dependent manner. However, TGFβ signaling inhibits NFE2L2 activity which can be counteracted by the administration of SFN. Finally, the fibroblast caveolae can also inhibit NFE2L2 function preventing the expression of antioxidant enzymes that require the translocation of a NFE2L2 transcription factor to the nucleus and its interaction with MAF.