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It modulates multiple signaling pathways, such as those involved in cell survival (Bcl-xL, Bcl-2, cFLIP, c-IAP1, XIAP), cell proliferation (cyclin D1, c-myc), tumor suppression (p53, p21), death receptor signaling (DR4, DR5), caspase activation (caspase-8, 3, 9), mitochondrial function, and protein kinase pathways (AKT, JNK, AMPK) [84]

After the model was expanded to include GS-H 2 Q adduct formation as a function of its reduction potential, it was then combined with the Reed glutathione model 21 in order to simulate how the quinone redox-metabolism of doxorubicin influenced the glutathione metabolism