ArticleThe Journal of biological chemistry2010
Regulation of NADPH oxidase activity in phagocytes: relationship between FAD/NADPH binding and oxidase complex assembly.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Molecular Views into the Synthesis and Activation of FlavocytochromeAntioxidants (Basel, Switzerland) · 2026Review
- Diphenyleneiodonium exhibits protective effects against both nociception and gastrointestinal inflammation in vivo.Inflammopharmacology · 2026Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Role of NADPH Oxidases in Stroke Recovery.Antioxidants (Basel, Switzerland) · 2024Review
- Structural basis for EROS binding to human phagocyte NADPH oxidase NOX2.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- CRISPR-gene-engineered CYBB knock-out PLB-985 cells, a useful model to study functional impact of X-linked chronic granulomatous disease mutations: application to the G412E X91+-CGD mutation.Clinical and experimental immunology · 2023Article
- Variant Type X91Journal of clinical immunology · 2022Article
- NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology.Antioxidants (Basel, Switzerland) · 2021Review
- Clinical, functional and genetic characterization of 16 patients suffering from chronic granulomatous disease variants - identification of 11 novel mutations in CYBB.Clinical and experimental immunology · 2021Article
- The "Biological Weapons" ofFrontiers in cellular and infection microbiology · 2021Review
- Interdomain Flexibility within NADPH Oxidase Suggested by SANS Using LMNG Stealth Carrier.Biophysical journal · 2020Article
- Article
- Down-regulation of NOX2 activity in phagocytes mediated by ATM-kinase dependent phosphorylation.Free radical biology & medicine · 2017Article
- Article
- Therapeutic effects of proteoliposomes on X-linked chronic granulomatous disease: proof of concept using macrophages differentiated from patient-specific induced pluripotent stem cells.International journal of nanomedicine · 2017Article
- Targeted redox inhibition of protein phosphatase 1 by Nox4 regulates eIF2α-mediated stress signaling.The EMBO journal · 2016Article
- Genetic disorders coupled to ROS deficiency.Redox biology · 2015Review
- Curly Encodes Dual Oxidase, Which Acts with Heme Peroxidase Curly Su to Shape the Adult Drosophila Wing.PLoS genetics · 2015Article
- Defects in NADPH Oxidase GenesCellular and molecular gastroenterology and hepatology · 2015Article
- Molecular characterization of LC3-associated phagocytosis reveals distinct roles for Rubicon, NOX2 and autophagy proteins.Nature cell biology · 2015Article
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7 authors at 4 institutions in 1 country.
Funding
Abstract
The X(+)-linked chronic granulomatous disease (X(+)-CGD) variants are natural mutants characterized by defective NADPH oxidase activity but with normal Nox2 expression. According to the three-dimensional model of the cytosolic Nox2 domain, most of the X(+)-CGD mutations are located in/or close to the FAD/NADPH binding regions. A structure/function study of this domain was conducted in X(+)-CGD PLB-985 cells exactly mimicking 10 human variants: T341K, C369R, G408E, G408R, P415H, P415L, Δ507QKT509-HIWAinsert, C537R, L546P, and E568K. Diaphorase activity is defective in all these mutants. NADPH oxidase assembly is normal for P415H/P415L and T341K mutants where mutation occurs in the consensus sequences of NADPH- and FAD-binding sites, respectively. This is in accordance with their buried position in the three-dimensional model of the cytosolic Nox2 domain. FAD incorporation is abolished only in the T341K mutant explaining its absence of diaphorase activity. This demonstrates that NADPH oxidase assembly can occur without FAD incorporation. In addition, a defect of NADPH binding is a plausible explanation for the diaphorase activity inhibition in the P415H, P415L, and C537R mutants. In contrast, Cys-369, Gly-408, Leu-546, and Glu-568 are essential for NADPH oxidase complex assembly. However, according to their position in the three-dimensional model of the cytosolic domain of Nox2, only Cys-369 could be in direct contact with cytosolic factors during oxidase assembly. In addition, the defect in oxidase assembly observed in the C369R, G408E, G408R, and E568K mutants correlates with the lack of FAD incorporation. Thus, the NADPH oxidase assembly process and FAD incorporation are closely related events essential for the diaphorase activity of Nox2.
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