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In conclusion, we show that APAP toxicity in HepG2 cells is largely independent of oxidative stress, and is linked instead to a decoupling of glycolysis from the TCA cycle, lactic acidosis, reduced NADPH production, and subsequent suppression of the anabolic pathways required for rapid growth

Exploiting nongenetic cell-to-cell variation for enhanced biosynthesis

Most of the mutants showed increased binding affinity, with S71pAcF and S26pAcF having the most significant improvements at 1.7 nM and 1.6 nM, representing a 9-fold increase compared to the wild type

and Skerra et al (1988) Science 240: 1038-1041)