ArticleThe Journal of biological chemistry2011
Kir4.1 channel expression is essential for parietal cell control of acid secretion.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- The physiological characteristics of inward rectifying potassium channel Kir4.2 and its research progress in human diseases.Frontiers in cell and developmental biology · 2025Review
- Metabolic regulator ERRγ governs gastric stem cell differentiation into acid-secreting parietal cells.Cell stem cell · 2024Article
- LRBA, a BEACH protein mutated in human immune deficiency, is widely expressed in epithelia, exocrine and endocrine glands, and neurons.Scientific reports · 2024Article
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- Article
- Claudin-18 Loss Alters Transcellular Chloride Flux but not Tight Junction Ion Selectivity in Gastric Epithelial Cells.Cellular and molecular gastroenterology and hepatology · 2021Article
- The Physiology of the Gastric Parietal Cell.Physiological reviews · 2020Review
- Physiological Significance of Ion Transporters and Channels in the Stomach and Pathophysiological Relevance in Gastric Cancer.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Gastric Parietal Cell Physiology and Helicobacter pylori-Induced Disease.Gastroenterology · 2019Review
- Kir2.1 is important for efficient BMP signaling in mammalian face development.Developmental biology · 2018Article
- Genetic ablation of carbonic anhydrase IX disrupts gastric barrier function via claudin-18 downregulation and acid backflux.Acta physiologica (Oxford, England) · 2018Article
- Chansporter complexes in cell signaling.FEBS letters · 2017Review
- Molecular aspects of structure, gating, and physiology of pH-sensitive background K2P and Kir K+-transport channels.Physiological reviews · 2015Review
- KIR4.1 Antibodies as Biomarkers in Multiple Sclerosis.Frontiers in neurology · 2014Article
- How Helicobacter pylori infection controls gastric acid secretion.Journal of gastroenterology · 2012Review
- KCNE2 and the K (+) channel: the tail wagging the dog.Channels (Austin, Tex.)Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kir4.1 channels were found to colocalize with the H(+)/K(+)-ATPase throughout the parietal cell (PC) acid secretory cycle. This study was undertaken to explore their functional role. Acid secretory rates, electrophysiological parameters, PC ultrastructure, and gene and protein expression were determined in gastric mucosae of 7-8-day-old Kir4.1-deficient mice and WT littermates. Kir4.1(-/-) mucosa secreted significantly more acid and initiated secretion significantly faster than WT mucosa. No change in PC number but a relative up-regulation of H(+)/K(+)-ATPase gene and protein expression (but not of other PC ion transporters) was observed. Electron microscopy revealed fully fused canalicular membranes and a lack of tubulovesicles in resting state Kir4.1(-/-) PCs, suggesting that Kir4.1 ablation may also interfere with tubulovesicle endocytosis. The role of this inward rectifier in the PC apical membrane may therefore be to balance between K(+) loss via KCNQ1/KCNE2 and K(+) reabsorption by the slow turnover of the H(+)/K(+)-ATPase, with consequences for K(+) reabsorption, inhibition of acid secretion, and membrane recycling. Our results demonstrate that Kir4.1 channels are involved in the control of acid secretion and suggest that they may also affect secretory membrane recycling.
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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.