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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
10.1016/j.bone.2016.11.025 39 ImuraA.TsujiY.MurataM.MaedaR.KubotaK.IwanoA.et al (2007)
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In metabolic diseases, the dysregulation of mitophagy and the ERAD/UPR contributes to insulin resistance and mitochondrial dysfunction
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