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A structure-based assignment of the glutathione activator site without transition-state analogues is much more difficult because of labile GSH interactions 2 that likely depend not only on the presence of the first glutathione moiety but also on conformational changes of the glutathionylated enzyme 3,12,37,44

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However, some mycotoxins suppress glutathione production

In athero-susceptible regions, activation of IRE1 and ATF6 is consistent with a high expression of molecular chaperones in ER

Release factors differing in specificity for terminator codons

Importantly, this metabolic derangement extends to the right ventricle, driving the cardiac transition from adaptive to maladaptive remodeling