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. Author manuscript; available in PMC: 2021 Jun 1.
Published in final edited form as: Nat Prod Rep. 2020 May 13;37(6):797–826. doi: 10.1039/c9np00061e

Figure 13. The GSK-3β/NRF2/β-TrCP regulatory axis.

Figure 13.

GSK-3β can phosphorylate the Neh6 domain of NRF2 making it an enhanced substrate for the CUL1/β-TrCP/RBX1 complex. GSK-3β is inhibited by Ser9 phosphorylation mediated by PKC or AKT/PKB, which are both activated by PDK1. AKT/PKB can also be activated by AMPK or inhibited by PHLPP2. PI3K converts PIP2 to PIP3, which activates PDK1. The action of PI3K can be reversed by PTEN. The letters A-D in the figure refer to sites of modulation by the compounds in Figure 14.