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Future studies will reveal the applicability of our model, for example, to activate enzymatically inactive glutaredoxins, to alter the sensitivity and responsiveness of glutaredoxin-coupled fluorescent redox sensors, to further address the catalytic mechanism with GSSCys, HEDS and physiological substrates, or to design specific transition-state inhibitors

In mouse model, Frakes et al

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Gut microbiomederived metabolites modulate intestinal epithelial cell damage and mitigate graft-versus-host disease

Gain of toxicity from ALS/FTD-linked repeat expansions in C9ORF72 is alleviated by antisense oligonucleotides targeting GGGGCC-containing RNAs