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These reactions are competitively inhibited by GSH, perhaps as a consequence of glutathionylation of the effected cysteine residues [96]

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Its molecular topology supports interactions with catalytic residues, allosteric regulatory surfaces, transmembrane helices, hydrophobic receptor pockets, nucleotidebinding cavities, redox-buffer modules and polymeric scaffolding proteinsenabling broad influence across metabolic, genomic, electrophysiological and structural regulatory networks