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Specific disulfide linkage between homocysteine and the sulfhydryl group of an intracellular protein may be an alternative molecular mechanism underlying hyperhomocysteinemia-induced vascular dysfunction

We used KEGG names, motifs, and PhosphoSitePlus (PSP) kinase/substrate annotations, and either the P -value or the BenjaminiHochberg FDR was set to 0.02 as a threshold

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This approach recognizes the complexity of sulfur metabolism and aims to address it in a more holistic and personalized manner

Stadnik J, Dolatowski ZJ, Baranowska HM