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This is consistent with our results showing that (i) the expression of Mck1p, the yeast homolog of GSK3, antagonizes the effect of CYS4 -OE in yeast (Figures 2AB) and (ii) the expression of a constitutively active form of GSK3 decreased H 2 S production in HepG2 cells (Figure 2G)

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Thus, copper toxicity may be a process that is dependent on GSH depletion, and indeed, increased concentrations of copper and dysregulation of copper homeostasis are observed in several neurodegenerative diseases in which GSH status is reduced, including Alzheimer's disease and models of ALS [54, 56]