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We show (i) that PfGrx-catalyzed redox reactions outcompete uncatalyzed reactions between roGFP2 and GSH or GSSG by several orders of magnitude, (ii) that the PfGrx-catalyzed reduction and oxidation of roGFP2 occur via a mono- and not a dithiol mechanism, and (iii) that the reduction of roGFP2(S 2 ) as a model non-glutathione disulfide substrate most likely involves a rate-limiting glutathionylation in a ternary complex with a GSH molecule that is activated at the 1st glutathione-interaction site of PfGrx

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Biallelic DNAJC3 Variants in a Neuroendocrine Developmental Disorder With Insulin Dysregulation

To further confirm RSL3-induced ferroptosis in EAAT3 and P65 knockdown cell lines, we performed TEM analysis, a classical imaging technique for detecting ferroptosis-related morphological changes