ArticleJournal of leukocyte biology2013
Identification of a region in p47phox/NCF1 crucial for phagocytic NADPH oxidase (NOX2) activation.
Article in Journal of leukocyte biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
- NADPH oxidase 2 (NOX2)-independent inducers of neutrophil extracellular traps promote resolution of chronic inflammation.Redox biology · 2026Article
- ThebioRxiv : the preprint server for biology · 2026Article
- Macrophage retrotransposon expression is associated with lupus.Genes and immunity · 2026Article
- Anti-Tumoral Treatment with Thioredoxin Reductase 1 Inhibitor Auranofin Fosters Regulatory T Cell and B16F10 Expansion in Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Intratumour oxidative hotspots provide a niche for cancer cell dissemination.Nature cell biology · 2025Article
- Whole-Exome Sequencing: Discovering Genetic Causes of Granulomatous Mastitis.International journal of molecular sciences · 2025Article
- Multifaceted Proteome Analysis at Solubility, Redox, and Expression Dimensions for Target Identification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- NCF4 regulates antigen presentation of cysteine peptides by intracellular oxidative response and restricts activation of autoreactive and arthritogenic T cells.Redox biology · 2024Article
- Human MHC Class II and Invariant Chain Knock-in Mice Mimic Rheumatoid Arthritis with Allele Restriction in Immune Response and Arthritis Association.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Antigen-presenting autoreactive B cells activate regulatory T cells and suppress autoimmune arthritis in mice.The Journal of experimental medicine · 2023Article
- Interferons as negative regulators of ILC2s in allergic lung inflammation and respiratory viral infections.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Human NCF1Antioxidants (Basel, Switzerland) · 2023Article
- NCF1-dependent production of ROS protects against lupus by regulating plasmacytoid dendritic cell development and functions.JCI insight · 2023Article
- Redox regulation of PTPN22 affects the severity of T-cell-dependent autoimmune inflammation.eLife · 2022Article
- Characterization of chronic relapsing antibody mediated arthritis in mice with a mutation in Ncf1 causing reduced oxidative burst.Molecular biomedicine · 2022Article
- Article
- NOX2 mediates quiescent handling of dead cell remnants in phagocytes.Redox biology · 2019Article
- Rapid spread of mannan to the immune system, skin and joints within 6 hours after local exposure.Clinical and experimental immunology · 2019Article
- Adaptations to high-intensity interval training in skeletal muscle require NADPH oxidase 2.Redox biology · 2019Article
- Mouse Models and Tools for theFrontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A point mutation in the mouse Ncf1(m1J) gene decreases production of ROS by the phagocytic NOX2 complex. Three mRNA splice variants are expressed, but only one is expressed as a protein, although at lower levels than the WT NCF1 (also known as p47phox). Our aim was to investigate whether the mutant p47phox, lacking 8 aa, is active, but as a result of its low expression, ROS production is decreased in Ncf1(m1J) mice, or whether the mutant p47phox completely lacks the capability to activate the NOX2 complex. The p47phox mutant (Δ228-235), which was equal to the protein in Ncf1(m1J) mice, failed to activate the NOX2 complex. When the deleted region was narrowed down to 2 aa, the p47phox protein remained inactive and failed to translocate to the membrane upon activation. Single amino acid substitutions revealed Thr233 to be vital for ROS production. Residues Tyr231 and Val232 also seemed to be important for p47phox function, as p47phox_Y231G and p47phox_V232G resulted in a >50% decrease in ROS production by the NOX2 complex. In addition, we identified the epitope of the D-10 anti-p47phox mAb. In conclusion, the p47phox protein variant expressed in Ncf1(m1J) mice is completely defective in activating the NOX2 complex to produce ROS, and the effect is dependent on SH3 region amino acids at positions 231-233, which are vital for the proper assembly of the NOX2 complex.
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