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Since GSH interacts with the 1st glutathione-interaction site, glutathionylated products of the random bi-uni mechanism might already adopt a suitable orientation as classical GSSR substrates for the subsequent deglutathionylation (Fig

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64,65 Tumors may also evade immune surveillance by downregulating tumor-associated antigens (TAAs), selecting for neoantigen-depleted clones, or upregulating alternative inhibitory checkpoints, as observed in EGFR-mutant non-small cell lung cancer (NSCLC) following targeted therapy

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