ArticleThe Journal of experimental medicine1995
The p47phox mouse knock-out model of chronic granulomatous disease.
Article in The Journal of experimental medicine, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 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
207 citing papers in PubMed, 490 citations in OpenAlex.
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- Knockout of p47phox inhibits deep vein thrombosis by regulating the PAC-1/FNG/MAC-1 signaling axis and ameliorating mitochondrial dysfunction.Frontiers in immunology · 2026Article
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- TNFα: TNFR1 signaling inhibits maturation and maintains the pro-inflammatory programming of monocyte-derived macrophages in murine chronic granulomatous disease.Frontiers in immunology · 2024Article
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- Neutrophils inhibit γδ T cell functions in the imiquimod-induced mouse model of psoriasis.Frontiers in immunology · 2022Article
- Granuloma Formation in aInternational journal of molecular sciences · 2021Article
- Macrophage Responses to Environmental Stimuli During Homeostasis and Disease.Endocrine reviews · 2021Article
- High-Intensity Interval Training and Moderate-Intensity Continuous Training Attenuate Oxidative Damage and Promote Myokine Response in the Skeletal Muscle of ApoE KO Mice on High-Fat Diet.Antioxidants (Basel, Switzerland) · 2021Article
- CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.Nature communications · 2021Article
- Oxidized CaMKII and O-GlcNAcylation cause increased atrial fibrillation in diabetic mice by distinct mechanisms.The Journal of clinical investigation · 2021Article
- High NaFrontiers in immunology · 2021Article
147 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic granulomatous disease (CGD) is caused by a congenital defect in phagocyte reduced nicotinamide dinucleotide phosphate (NADPH) oxidase production of superoxide and related species. It is characterized by recurrent life-threatening bacterial and fungal infections and tissue granuloma formation. We have created a mouse model of CGD by targeted disruption of p47phox, one of the genes in which mutations cause human CGD. Identical to the case in human CGD, leukocytes from p47phox-/- mice produced no superoxide and killed staphylococci ineffectively. p47phox-/- mice developed lethal infections and granulomatous inflammation similar to those encountered in human CGD patients. This model mirrors human CGD and confirms a critical role for the phagocyte NADPH oxidase in mammalian host defense.
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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.