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S-glutathionylation of PDI. Nitrosative stress from an exogenous agent (PABA/NO) increases intracellular NO and leads to the production of SNO-PDI. However, this may result in a decrease in GSSG/GSH ratio and increases in the free cellular pool of GSH. GSH then binds to the catalytic (a, a′) domains of PDI, resulting in S-glutathionylation (P-SSG) of its cysteine residues and attenuation of its protective isomerase and chaperone activity.
