ArticleThe Journal of clinical investigation1994
Activation of H+ conductance in neutrophils requires assembly of components of the respiratory burst oxidase but not its redox function.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
- Voltage-Gated Proton Channels as Novel Drug Targets: From NADPH Oxidase Regulation to Sperm Biology.Antioxidants & redox signaling · 2015Review
- A contribution to the history of the proton channel.Wiley interdisciplinary reviews. Membrane transport and signaling · 2012Article
- The intimate and mysterious relationship between proton channels and NADPH oxidase.FEBS letters · 2009Article
- Voltage-gated proton channels: what's next?The Journal of physiology · 2008Review
- Expression of Nox1 in 3T3 cells increases cellular acid production but not proton conductance.Archives of biochemistry and biophysics · 2007Article
- Interactions between electron and proton currents in excised patches from human eosinophils.The Journal of general physiology · 2003Article
- NOX family NADPH oxidases: do they have built-in proton channels?The Journal of general physiology · 2002Review
- Voltage-gated proton "channels": a spectator's viewpoint.The Journal of general physiology · 2002Review
- The gp91phox component of NADPH oxidase is not a voltage-gated proton channel.The Journal of general physiology · 2002Review
- Activation of NADPH oxidase-related proton and electron currents in human eosinophils by arachidonic acid.The Journal of physiology · 2001Article
- Chronic granulomatous disease.Clinical and experimental immunology · 2000Review
- A novel H(+) conductance in eosinophils: unique characteristics and absence in chronic granulomatous disease.The Journal of experimental medicine · 1999Article
- Na+/H+ exchange activity during phagocytosis in human neutrophils: role of Fcgamma receptors and tyrosine kinases.The Journal of cell biology · 1996Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In phagocytes, superoxide generation by the NADPH oxidase is accompanied by metabolic acid production. Cytoplasmic acidification during this metabolic burst is prevented by a combination of H+ extrusion mechanisms, including a unique H+ conductance. NADPH oxidase is deficient in chronic granulomatous disease (CGD) patients. The burst of acid production is absent in CGD patients lacking the 47-kD (p47-phox) or the 91-kD (gp91-phox) subunits of the oxidase. Activation of the H+ conductance is also defective in these patients suggesting that (a) the oxidase itself undertakes H+ translocation or (b) oxidase assembly is required to stimulate a separate H+ conducting entity. To discern between these possibilities, three rare forms of CGD were studied. In neutrophils expressing nonfunctional cytochrome b, the conductance was activated to near-normal levels, implying that functional oxidase is not required to activate H+ extrusion. CGD cells expressing diminished amounts of cytochrome displayed H+ conductance approaching normal levels, suggesting that the oxidase itself does not translocate H+. Finally, the conductance was only partially inhibited in patients lacking the 67-kD subunit, indicating that this component is not essential for stimulation of H+ transport. We propose that normal assembly of the oxidase subunits is required for optimal activation of a closely associated but distinct H+ conducting entity.
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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.