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Similarly, the same effect was observed in DLBCL cells with endogenous levels of GSH and the extent of GSH depletion was comparable to GSH depletion as a result of GSH synthesis inhibition using the -glutamylcysteine synthetase (-GCS) inhibitor buthionine sulphoximine (BSO) (Fig

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Peroxiredoxin 5: Structure, mechanism, and function of the mammalian atypical 2-Cys peroxiredoxin

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2E), hepatocytes failed to activate caspases in response to APAP, in vitro and in vivo (Fig

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