ArticleThe Biochemical journal1996
Detection of gp91-phox precursor protein in B-cell lines from patients with X-linked chronic granulomatous disease as an indicator for mutations impairing cytochrome b558 biosynthesis.
Article in The Biochemical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 31 citations in OpenAlex.
- EROS is a selective chaperone regulating the phagocyte NADPH oxidase and purinergic signalling.eLife · 2022Article
- Variant Type X91Journal of clinical immunology · 2022Article
- Monocyte/macrophage-specific NADPH oxidase contributes to antimicrobial host defense in X-CGD.Journal of clinical immunology · 2015Article
- A highly sensitive chemiluminescence assay for superoxide detection and chronic granulomatous disease diagnosis.Tropical medicine and health · 2011Article
- Germline CYBB mutations that selectively affect macrophages in kindreds with X-linked predisposition to tuberculous mycobacterial disease.Nature immunology · 2011Article
- Hematologically important mutations: X-linked chronic granulomatous disease (third update).Blood cells, molecules & diseases · 2010Review
- Genetics and immunopathology of chronic granulomatous disease.Seminars in immunopathology · 2008Review
- Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.Journal of clinical pathology · 2003Article
- Analysis of glycosylation sites on gp91phox, the flavocytochrome of the NADPH oxidase, by site-directed mutagenesis and translation in vitro.The Biochemical journal · 1997Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NADPH oxidase cytochrome b558 consists of two subunits, gp91-phox and p22-phox, defects of which result in chronic granulomatous disease (CGD). The nature of the interaction between these subunits has yet to be determined. Absence of p22-phox in autosomal CGD patient-derived B-cell lines results in detectable levels of an incompletely glycosylated gp91-phox precursor. We have detected this same precursor species in four cell lines from patients with the X-linked form of the disease due to mutations in gp91-phox. Such mutations should delineate regions of gp91-phox important for its biosynthesis, including stable association with p22-phox. One mutation mapped to the putative FAD-binding domain, one mapped to a potential haem-binding domain, and two involved the region encoded by exon 3.
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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.