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. 2022 Feb 2;9:809952. doi: 10.3389/fcell.2021.809952

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Copyright © 2022 Gao, Guo, Yang, Wang, Xia, Gong, Zhang and Yan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Keap1-dependent and -independent regulation of Nrf2. (A) Keap1-dependent Nrf2 regulation. Under normal conditions, Nrf2 is sequestered in the cytoplasm by Keap1. Under oxidative stress, Nrf2 dissociates from Keap1, translocates to the nucleus and activates the ARE-gene battery. (B) Keap1-independent Nrf2 regulation. Phosphorylation of Nrf2 by GSK facilitates the recognition of Nrf2 by β-TrCP for CUL1-mediated ubiquitination and subsequent proteasome degradation. (C) P62-dependent Nrf2 regulation. p62 is sequestered with Keap1 and increased Nrf2 signaling. Abbreviations: Keap1, Kelch-like ECH-associated protein 1; Nrf2, Nuclear Factor Erythroid (NF-E2)-Related Factor 2; ARE, antioxidant response element; GSK-3, Glycogen synthase kinase 3; β-TrCP, β-transducin repeat-containing protein; Ub, ubiquitin.