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. 2021 Dec 21;11(1):8. doi: 10.3390/antiox11010008

Figure 1.

Figure 1

Schematic of canonical factors in cell-autonomous sources of oxidative stress and response are shown in (a). At basal state, transcription factor NRF2 is sequestered in the nucleus by the KEAP1 ubiquitination complex; here, CUL3 ligase activity leads to poly-ubiquitination of NRF2 for its targeted proteasomal degradation. Oxidative stress leads to a conformational change in KEAP1, and NRF2 is released to be phosphorylated and translocated into the nucleus to activate antioxidant response gene programs. Examples of non-cell-autonomous mediators of oxidative stress are shown in (b). Created with BioRender.com (accessed on 21 October 2021).