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Thiols, especially cysteine residues in proteins, serve as significant targets for ROS/RNS-mediated signaling because of their capacity for reversible oxidation

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Since glutamate-cysteine ligase catalytic subunit (GCLC) and NAD(P)H quinone dehydrogenase 1 (NQO1) are key regulators of GSH biosynthesis and oxidative stress resistance, we hypothesized that SYNCRIP might influence ferroptosis through modulation of glutathione metabolism [23, 24]