ArticleThe Biochemical journal2010
The myeloperoxidase-derived oxidant HOSCN inhibits protein tyrosine phosphatases and modulates cell signalling via the mitogen-activated protein kinase (MAPK) pathway in macrophages.
Article in The Biochemical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 84 citations in OpenAlex.
- Factors governing the response ofFrontiers in cellular and infection microbiology · 2026Review
- An Optimized Protocol for Enzymatic Hypothiocyanous Acid Synthesis.Methods and protocols · 2025Article
- The Roles of Neutrophil-Derived Myeloperoxidase (MPO) in Diseases: The New Progress.Antioxidants (Basel, Switzerland) · 2024Review
- Myeloperoxidase: Regulation of Neutrophil Function and Target for Therapy.Antioxidants (Basel, Switzerland) · 2022Review
- Hypochlorous Acid Chemistry in Mammalian Cells-Influence on Infection and Role in Various Pathologies.International journal of molecular sciences · 2022Review
- Hypocrates is a genetically encoded fluorescent biosensor for (pseudo)hypohalous acids and their derivatives.Nature communications · 2022Article
- Hypochlorous Acid: From Innate Immune Factor and Environmental Toxicant to Chemopreventive Agent Targeting Solar UV-Induced Skin Cancer.Frontiers in oncology · 2022Review
- Fluorescent Probes for Selective Recognition of Hypobromous Acid: Achievements and Future Perspectives.Molecules (Basel, Switzerland) · 2021Review
- The effects of neutrophil-generated hypochlorous acid and other hypohalous acids on host and pathogens.Cellular and molecular life sciences : CMLS · 2021Review
- Network Medicine-Based Unbiased Disease Modules for Drug and Diagnostic Target Identification in ROSopathies.Handbook of experimental pharmacology · 2021Article
- The Role of Inflammation and Myeloperoxidase-Related Oxidative Stress in the Pathogenesis of Genetically Triggered Thoracic Aortic Aneurysms.International journal of molecular sciences · 2020Review
- Molecular Targets in Alzheimer's Disease.Molecular neurobiology · 2019Review
- Intracellular IL-37b interacts with Smad3 to suppress multiple signaling pathways and the metastatic phenotype of tumor cells.Oncogene · 2017Article
- Pre-steady-state Kinetics Reveal the Substrate Specificity and Mechanism of Halide Oxidation of Truncated Human Peroxidasin 1.The Journal of biological chemistry · 2017Article
- CVD and Oxidative Stress.Journal of clinical medicine · 2017Review
- An immunochemical approach to detect oxidized protein tyrosine phosphatases using a selective C-nucleophile tag.Molecular bioSystems · 2016Article
- Biochemical mechanisms and therapeutic potential of pseudohalide thiocyanate in human health.Free radical research · 2015Review
- The Role of Reactive Oxygen Species (ROS) in the Formation of Extracellular Traps (ETs) in Humans.Biomolecules · 2015Review
- Hypothiocyanous acid oxidation of tubulin cysteines inhibits microtubule polymerization.Archives of biochemistry and biophysics · 2014Article
- Selenocysteine confers resistance to inactivation by oxidation in thioredoxin reductase: comparison of selenium and sulfur enzymes.Biochemistry · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MPO (myeloperoxidase) catalyses the oxidation of chloride, bromide and thiocyanate by hydrogen peroxide to HOCl (hypochlorous acid), HOBr (hypobromous acid) and HOSCN (hypothiocyanous acid) respectively. Specificity constants indicate that SCN- is a major substrate for MPO. HOSCN is also a major oxidant generated by other peroxidases including salivary, gastric and eosinophil peroxidases. While HOCl and HOBr are powerful oxidizing agents, HOSCN is a less reactive, but more specific, oxidant which targets thiols and especially low pKa species. In the present study we show that HOSCN targets cysteine residues present in PTPs (protein tyrosine phosphatases) with this resulting in a loss of PTP activity for the isolated enzyme, in cell lysates and intact J774A.1 macrophage-like cells. Inhibition also occurs with MPO-generated HOCl and HOBr, but is more marked with MPO-generated HOSCN, particularly at longer incubation times. This inhibition is reversed by dithiothreitol, particularly at early time points, consistent with the reversible oxidation of the active site cysteine residue to give either a cysteine-SCN adduct or a sulfenic acid. Inhibition of PTP activity is associated with increased phosphorylation of p38a and ERK2 (extracellular-signal-regulated kinase 2) as detected by Western blot analysis and phosphoprotein arrays, and results in altered MAPK (mitogen-activated protein kinase) signalling. These data indicate that the highly selective targeting of some protein thiols by HOSCN can result in perturbation of cellular phosphorylation and altered cell signalling. These changes occur with (patho)physiological concentrations of SCN- ions, and implicate HOSCN as an important mediator of inflammation-induced oxidative damage, particularly in smokers who have elevated plasma levels of SCN-.
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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.