Some of the phosphorylation sites that have been subjected to the greatest degree of study are Ser40, Ser44, Ser579, Ser585, Ser592, Ser616, Ser637, Ser656, Ser693, and other phosphorylation sites (Qi et al., 2019)
In addition, GSSG retained in mitochondria during oxidative stress can lead to the S-gluthionylation of target proteins with mitochondrial dysfunction (20, 21)
One possible explanation for such a response is that inhibition of mTORC1 and activation of GCN2 collectively suppresses global translation to conserve nutrients, while selective translation of mRNA such as ATF4 (mediated by increased p-eIF2) activates the expression of AARE genes to mitigate cellular stress
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