A Molecular Redox Switch on p21ras

摘要: We have identified the site of molecular interaction between nitric oxide (NO) and p21ras responsible for initiation signal transduction. found that was singly S-nitrosylated localized this modification to a fragment containing Cys118. A mutant form p21ras, in which Cys118 changed serine residue termed p21rasC118S, not S-nitrosylated. NO-related species stimulated guanine nucleotide exchange on wild-type resulting an active form, but p21rasC118S. Furthermore, contrast parental Jurkat T cells, did stimulate mitogen-activated protein kinase activity cells transfected with These data indicate is critical redox regulation S-nitrosylation triggers downstream signaling.