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lnterleukin-16: the ins and outs of regulating T-cell activation

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While the cysteine decomposition is coupled with mitochondrial bioenergetics in the cells with intact KEAP1-NRF2 system, in NRF2-addicted cancer cells, most of the available cysteine appears to flow into the anabolic pathway, namely, glutathione synthesis and leaves the catabolic pathway in mitochondria, which is consistent with the observation that mitochondrial respiration is limited in NRF2-addicted cancer cells (Sayin et al

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Simultaneously, the significantly diminished proportion of Fe 3+ /Fe 2+ ratio further indicated that UPFB was utilized to exhaust GSH through a redox reaction (Figure 7F)

Use of a systems model of drug-induced liver injury (DILIsym()) to elucidate the mechanistic differences between acetaminophen and its less-toxic isomer, AMAP, in mice