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However, owing to the largely conserved reaction mechanism of GS and by extension, largely conserved active site residues (Figure 1), many of these inhibitors act broadly on GS homologues or isoforms suggesting that future development of nonorthosteric inhibitors may be fruitful and may be inspired by natural mechanisms that regulate GS activity

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Under conditions of elevated oxidative stress, an altered cellular redox state can trigger the release of zinc from metallothioneins through sulfide/disulfide exchange mechanisms (Jiang et al., 1998[216])