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The contribution of homocysteine metabolism disruption to endothelial dysfunction: State-of-the-art

If that methionine residue plays a role in receptor binding or biological activity, oxidation can reduce or eliminate the peptide effect entirely

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Furthermore, the administration of S-biAb/dEGCG@NPs not only strengthens IFN-mediated tumorcidal efficacy by targeting B7-H3 which prevents T cell activation, but also significantly downregulates GPX4, intensely boosting the capacity of immune checkpoint blockage therapy[175]