ArticleCirculation research2012
Measurement of S-nitrosylation occupancy in the myocardium with cysteine-reactive tandem mass tags: short communication.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Differential alkylation-based redox proteomics--Lessons learnt.Redox biology · 2015Pooled it
- Protein S-Nitrosylation in Heart Failure: A Compartment-Resolved Review of Mechanisms, Evidence Boundaries, and Translational Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- The Role of Protein S-Nitrosylation in Mitochondrial Quality Control in Central Nervous System Diseases.Aging and disease · 2024Review
- Oxidative Post-translational Protein Modifications upon Ischemia/Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2024Article
- Chemoproteomic strategy identified p120-catenin glutathionylation regulates E-cadherin degradation and cell migration.Cell chemical biology · 2023Article
- Hsp70 in Redox Homeostasis.Cells · 2022Review
- Organic mercury solid phase chemoselective capture for proteomic identification of S-nitrosated proteins and peptides.Nitric oxide : biology and chemistry · 2021Article
- Protein S-nitrosylation and oxidation contribute to protein misfolding in neurodegeneration.Free radical biology & medicine · 2021Review
- Aortic disease in Marfan syndrome is caused by overactivation of sGC-PRKG signaling by NO.Nature communications · 2021Article
- Implications of Oxidative and Nitrosative Post-Translational Modifications in Therapeutic Strategies against Reperfusion Damage.Antioxidants (Basel, Switzerland) · 2021Review
- Pharmacological Inhibition of S-Nitrosoglutathione Reductase Reduces Cardiac Damage Induced by Ischemia-Reperfusion.Antioxidants (Basel, Switzerland) · 2021Article
- Post-Translational S-Nitrosylation of Proteins in Regulating Cardiac Oxidative Stress.Antioxidants (Basel, Switzerland) · 2020Review
- A knock-in mutation at cysteine 144 of TRIM72 is cardioprotective and reduces myocardial TRIM72 release.Journal of molecular and cellular cardiology · 2019Article
- Integrated Dissection of Cysteine Oxidative Post-translational Modification Proteome During Cardiac Hypertrophy.Journal of proteome research · 2018Article
- S-Nitrosoglutathione Reductase Is Essential for Protecting the Female Heart From Ischemia-Reperfusion Injury.Circulation research · 2018Article
- Precision Profiling of the Cardiovascular Post-Translationally Modified Proteome: Where There Is a Will, There Is a Way.Circulation research · 2018Review
- Quantitative proteomic characterization of redox-dependent post-translational modifications on protein cysteines.Molecular bioSystems · 2017Review
- Article
- Proteomics Research in Cardiovascular Medicine and Biomarker Discovery.Journal of the American College of Cardiology · 2016Review
- Chemoproteomic Strategy to Quantitatively Monitor Transnitrosation Uncovers Functionally Relevant S-Nitrosation Sites on Cathepsin D and HADH2.Cell chemical biology · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleS-nitrosylation (SNO) is a reversible, thiol-based protein modification that plays an important role in the myocardium by protecting critical cysteine residues from oxidation. However, little is known with regard to the percentage of a given protein that is modified by SNO (ie, SNO occupancy). Current methods allow for the relative quantification of SNO levels, but not for the determination of SNO occupancy.
objectiveTo develop a method for the measurement of SNO occupancy, and apply this methodology to determine SNO occupancy in the myocardium. METHODS AND
resultsWe developed a differential cysteinereactive tandem mass tag (cysTMT) labeling procedure for the measurement of SNO occupancy. To validate this cysTMT labeling method, we treated whole-heart homogenates with the S-nitrosylating agent S-nitrosoglutathione and determined maximal SNO occupancy. We also examined SNO occupancy under more physiological conditions and observed that SNO occupancy is low for most protein targets at baseline. Following ischemic preconditioning, SNO occupancy increased to an intermediate level compared to baseline and Snitrosoglutathione treatment, and this is consistent with the ability of SNO to protect against cysteine oxidation.
conclusionsThis novel cysTMT labeling approach provides a method for examining SNO occupancy in the myocardium. Using this approach, we demonstrated that IPC-induced SNO occupancy levels are sufficient to protect against oxidation.
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