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The timepoint chosen (when drug-tolerant cells are emerging after treatment) probably contributes to this effect, and later timepoints (when cells perhaps enter senescence or other more terminally arrested states) are more likely to reflect the expected gene expression patterns
We talked a little bit about the glutathione, but there's also ones that are involved in airborne carcinogens like benzene
17 They also downregulate CD36 (fatty acid translocase), reducing hepatocyte fatty acid uptake, and they upregulate bile acid metabolism
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