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3g, GS siRNA transfection, which led to more than 60% GS gene silencing, similarly increased the sensitivity of hepatocytes to TNF killing, suggesting that increased GSSG accumulation mechanistically contributed to cellular glutathione imbalance-induced susceptibility to TNF-induced cell death

[12] The glutathione molecule binds in a cleft between N - and C -terminal domains - the catalytically important residues are proposed to reside in the N -terminal domain