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. 2016 Apr 26;163:1–23. doi: 10.1016/j.pharmthera.2016.03.018

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© 2016 Elsevier Inc. All rights reserved.

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Fig. 3 — General regulatory pathway of PRDX expression. Nrf2 induces the expression of PRDXs in response to oxidative and electrophilic stresses. Under unstressed conditions, Nrf2 is degraded via the ubiquitin (Ub)–proteasome pathway in a Keap1-dependent manner. The Keap1 homodimer binds a single Nrf2 molecule through two-site binding utilizing the DLG and ETGE motifs. When Nrf2 inducers inactivate Keap1 via the modification of cysteine residues (Cys) under oxidative stress and electrophiles modified condition, Nrf2 is stabilized, and de novo synthesized Nrf2 translocates into the nucleus. Nrf2 heterodimerizes with small Maf proteins (sMaf) and activates the expression of target genes including PRDXs through antioxidant response elements (AREs), exerting cytoprotective effects against various diseases and toxic insults. Phosphorylation of Nrf2 by various kinases has also been implicated in the liberation, stability, and trans-activation of Nrf2.