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We propose that the requirement of two distinct glutathione interaction sites for the efficient reduction of glutathionylated disulfide substrates explains the deviating structure–function relationships, activities and substrate preferences of different glutaredoxin subfamilies as well as thioredoxins

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This is consistent with our hypothesis that this group would include patients in whom excitotoxic damage during acute florid illness has led to subsequent reductions in mental and neural activity mediated by glutamatergic neurotransmission [3, 4]