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Mutation of these AMPK sites on TSC2 to non-phosphorylatable alanine residues offset, in part, the attenuation of mTORC1 substrate p70 ribosomal S6 kinase 1 (S6K1) and eIF4E-binding protein 1 (4E-BP1) phosphorylation after AMPK activation by 2-deoxyglucose (2-DG) treatment, an inhibitor of glycolysis [24]

Building on this idea, we further pushed the boundaries by combining an N-terminal Rex domain from NAPstar4, a NAPstar variant initially dismissed due to a lack of detectable affinity for NADPH (Fig

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Additionally, the autoimmune disease also appears to be hallmarked by imbalanced glutathione levels.15 Rebalancing glutathione levels can restore immune system competence and bring chronic inflammation under better control

SKN-1 regulation can be bypassed by inactivating WDR-23, which normally drives SKN-1 to proteasomal degradation under non-stressed conditions 20