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Submitted on December 6, 2004
Pharmacology, University of Minnesota Medical School, Minneapolis, Mn 55455
Corresponding Author: weixx009{at}umn.edu
Nitric oxide (NO) is an important factor that induces post-translational-modifications of proteins by cellular reduction and oxidation mechanism: cysteinyl-nitrosylation or tyrosine (Tyr) nitration. NF-kB activity can be rapidly suppressed by sodium nitroprusside (SNP), a NO donor. This effect was effectively reversed by peroxynitrite scavenger deferoxamine, suggesting a Tyr nitration-mediated mechanism. Western blot with nitrotyrosine specific antibody demonstrated that the p65 subunit of NF-kB was predominantly nitrated on Tyr residues. Tyr-nitration of p65 induced its dissociation from p50, its association with IkBa and subsequent sequestration of p65 in the cytoplasm by IkBa-mediated export. Liquid chromatography-coupled nanoelectrospray mass spectrometry revealed specific nitration on Tyr-66 and Tyr-152 residues of p65. Mutation studies confirmed that both Tyr-66 and Tyr-152 residues were important for the direct effects of NO on p65, which resulted in more p65 export and inactivation of NF-kB activity. This study identified a novel and efficient pathway where NO rapidly inactivated NF-kB activity by inducing Tyr-nitration on p65.
Revised on January 15, 2005
Accepted on January 18, 2005
Tyrosine nitration on p65: a novel mechanism to rapidly inactivate NF-kB
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