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As Lushchak [60] discussed, inhibition of glutathione reductase, phosphofructokinase, fatty acid synthase, or activation of fructose-1,6-bisphosphatase by CoASSG was shown

The researchers reasoned, therefore, that TGR might be an essential parasite protein and a potentially important drug target

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This was paralleled by the accumulation of glucose-6-phosphate (6P) in steady state GSH-deficient FoB (Supplementary Fig