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. 2018 Nov 22;20:526–532. doi: 10.1016/j.redox.2018.11.011

Fig. 4.

Fig. 4

Putative model for LGG regulation of ROS production in the gut epithelium. Rac1 is first activated following LGG stimulation of Formyl Peptide Receptor. Rac1 subsequently becomes palmitoylated at C178 and localized at the plasma membrane, where it activates Nox-1 to generate ROS. Endocytosis of this complex forms a redoxosome that generates elevated levels of ROS. In a feedback loop, further palmitoylation of Rac-1 is blocked by oxidation of C178, decreasing the formation of redoxosomes.