ArticleBiochemistry2012
Mechanism and kinetics of inducible nitric oxide synthase auto-S-nitrosation and inactivation.
Article in Biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Key roles of GAPDH, Hsp90, and NO in heme trafficking.Journal of inorganic biochemistry · 2026Review
- Vitamin DExperimental biology and medicine (Maywood, N.J.) · 2025Article
- Biopterin metabolism and nitric oxide recoupling in cancer.Frontiers in oncology · 2023Review
- New roles for GAPDH, Hsp90, and NO in regulating heme allocation and hemeprotein function in mammals.Biological chemistry · 2022Review
- S-Nitroso-l-cysteine and ventilatory drive: A pediatric perspective.Pediatric pulmonology · 2022Review
- Nitric oxide and the brain. Part 2: Effects following neonatal brain injury-friend or foe?Pediatric research · 2021Review
- Nitric Oxide-Releasing Hyaluronic Acid as an Antibacterial Agent for Wound Therapy.Biomacromolecules · 2021Article
- Regulation of cytochrome P450 enzyme activity and expression by nitric oxide in the context of inflammatory disease.Drug metabolism reviews · 2020Review
- Inducible nitric oxide synthase: Regulation, structure, and inhibition.Medicinal research reviews · 2020Review
- Agmatine Prevents Oxidative-nitrative Stress in Blood Leukocytes Under Streptozotocin-induced Diabetes Mellitus.Open life sciences · 2019Article
- Thiol-Based Redox Modulation of Soluble Guanylyl Cyclase, the Nitric Oxide Receptor.Antioxidants & redox signaling · 2017Review
- Mechanism of Sirt1 NAD+-dependent Protein Deacetylase Inhibition by Cysteine S-Nitrosation.The Journal of biological chemistry · 2016Article
- A substrate trapping approach identifies proteins regulated by reversible S-nitrosylation.Molecular & cellular proteomics : MCP · 2014Article
- Fourier transform infrared spectroscopy study of ligand photodissociation and migration in inducible nitric oxide synthase.F1000Research · 2014Article
- Nitrosothiols in the immune system: signaling and protection.Antioxidants & redox signaling · 2013Review
- S-nitrosylation: integrator of cardiovascular performance and oxygen delivery.The Journal of clinical investigation · 2013Review
- Mechanisms of S-nitrosothiol formation and selectivity in nitric oxide signaling.Current opinion in chemical biology · 2012Review
- A Conspectus of Cellular Mechanisms of Nitrosothiol Formation from Nitric Oxide.Forum on immunopathological diseases and therapeutics · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Nitric oxide (NO), the product of the nitric oxide synthase (NOS) reaction, was previously shown to result in S-nitrosation of the NOS Zn(2+)-tetrathiolate and inactivation of the enzyme. To probe the potential physiological significance of NOS S-nitrosation, we determined the inactivation time scale of the inducible NOS isoform (iNOS) and found it directly correlates with an increase in the level of iNOS S-nitrosation. A kinetic model of NOS inactivation in which arginine is treated as a suicide substrate was developed. In this model, NO synthesized at the heme cofactor is partitioned between release into solution (NO release pathway) and NOS S-nitrosation followed by NOS inactivation (inactivation pathway). Experimentally determined progress curves of NO formation were fit to the model. The NO release pathway was perturbed through addition of the NO traps oxymyoglobin (MbO(2)) and β2 H-NOX, which yielded partition ratios between NO release and inactivation of ~100 at 4 μM MbO(2) and ~22000 at saturating trap concentrations. The results suggest that a portion of the NO synthesized at the heme cofactor reacts with the Zn(2+)-tetrathiolate without being released into solution. Perturbation of the inactivation pathway through addition of the reducing agent GSH or TCEP resulted in a concentration-dependent decrease in the level of iNOS S-nitrosation that directly correlated with protection from iNOS inactivation. iNOS inactivation was most responsive to physiological concentrations of GSH with an apparent K(m) value of 13 mM. NOS turnover that leads to NOS S-nitrosation might be a mechanism for controlling NOS activity, and NOS S-nitrosation could play a role in the physiological generation of nitrosothiols.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.