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Shami et al., 2003] were selectively activated by GST M1 and GST A1, respectively, and produced abundant NO in the tumor and contributed to chemotherapy by GSH consumption, DNA synthesis inhibition and inhibition of enzymes responsible for cellular damage repair ( Figure 2E )
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PERK-dependent activation of Nrf2 contributes to redox homeostasis and cell survival following endoplasmic reticulum stress
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