ArticleNature2004
The large-conductance Ca2+-activated K+ channel is essential for innate immunity.
Article in Nature, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 67 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
67 citing papers in PubMed, 201 citations in OpenAlex.
- Factors governing the response ofFrontiers in cellular and infection microbiology · 2026Review
- NS1619 Alleviate Brain-Derived Extracellular Vesicle-Induced Brain Injury by Regulating BKca Channel and Nrf2/HO-1/NF-ĸB Pathway.Oxidative medicine and cellular longevity · 2022Article
- α-Hemolysin of uropathogenic E. coli regulates NLRP3 inflammasome activation and mitochondrial dysfunction in THP-1 macrophages.Scientific reports · 2020Article
- A lysosomal KScientific reports · 2020Article
- Airway Mucins Inhibit Oxidative and Non-Oxidative Bacterial Killing by Human Neutrophils.Frontiers in pharmacology · 2020Article
- Thioridazine: A Non-Antibiotic Drug Highly Effective, in Combination with First Line Anti-Tuberculosis Drugs, against Any Form of Antibiotic Resistance of Mycobacterium tuberculosis Due to Its Multi-Mechanisms of Action.Antibiotics (Basel, Switzerland) · 2017Review
- Streptolysin O Rapidly Impairs Neutrophil Oxidative Burst and Antibacterial Responses to Group A Streptococcus.Frontiers in immunology · 2015Article
- Article
- Big Potassium (BK) ion channels in biology, disease and possible targets for cancer immunotherapy.International immunopharmacology · 2014Review
- Integrative Approach for Computationally Inferring Interactions between the Alpha and Beta Subunits of the Calcium-Activated Potassium Channel (BK): a Docking Study.Bioinformatics and biology insights · 2013Article
- What really happens in the neutrophil phagosome?Free radical biology & medicine · 2012Review
- Large conductance, calcium- and voltage-gated potassium (BK) channels: regulation by cholesterol.Pharmacology & therapeutics · 2012Review
- Splicing of the rSlo gene affects the molecular composition and drug response of Ca2+-activated K+ channels in skeletal muscle.PloS one · 2012Article
- Regulation of reactive oxygen species generation in cell signaling.Molecules and cells · 2011Review
- Retracted science and the retraction index.Infection and immunity · 2011Article
- Current commentary: Can free radicals be good for you?Science progress · 2011Article
- The many roles of NOX2 NADPH oxidase-derived ROS in immunity.Seminars in immunopathology · 2010Review
- Increasing reactive oxygen species as a therapeutic approach to treat hereditary leiomyomatosis and renal cell carcinoma.Cell cycle (Georgetown, Tex.) · 2010Article
- VSOP/Hv1 proton channels sustain calcium entry, neutrophil migration, and superoxide production by limiting cell depolarization and acidification.The Journal of experimental medicine · 2010Article
- A role for BK channels in heart rate regulation in rodents.PloS one · 2010Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2010-11-04Investigation by Company/Institution · Results Not Reproducible · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Neutrophil leukocytes have a pivotal function in innate immunity. Dogma dictates that the lethal blow is delivered to microbes by reactive oxygen species (ROS) and halogens, products of the NADPH oxidase, whose impairment causes immunodeficiency. However, recent evidence indicates that the microbes might be killed by proteases, activated by the oxidase through the generation of a hypertonic, K+-rich and alkaline environment in the phagocytic vacuole. Here we show that K+ crosses the membrane through large-conductance Ca2+-activated K+ (BK(Ca)) channels. Specific inhibitors of these channels, iberiotoxin and paxilline, blocked oxidase-induced 86Rb+ fluxes and alkalinization of the phagocytic vacuole, whereas NS1619, a BK(Ca) channel opener, enhanced both. Characteristic outwardly rectifying K+ currents, reversibly inhibited by iberiotoxin, were demonstrated in neutrophils and eosinophils and the expression of the alpha-subunit of the BK channel was confirmed by western blotting. The channels were opened by the combination of membrane depolarization and elevated Ca2+ concentration, both consequences of oxidase activity. Remarkably, microbial killing and digestion were abolished when the BK(Ca) channel was blocked, revealing an essential and unexpected function for this K+ channel in the microbicidal process.
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What OpenQuestion holds
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.