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Taken together, these results suggest regulation of GS may also be important in determining the overall GSH synthetic capacity under certain conditions and especially in non-hepatic tissues

Reversible sequestration of active site cysteines in a 2Fe-2S-bridged dimer provides a mechanism for glutaredoxin 2 regulation in human mitochondria

Conclusion: These results suggest that the Notch1 signaling pathway acts as an upstream regulator of DEGs and can be a target to regulate the changes involved with endothelial mitochondrial dysfunction-dependent BBB disruption