ArticleThe Journal of physiology2009
KCNQ1 is the luminal K+ recycling channel during stimulation of gastric acid secretion.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 45 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
- KCNQ1 is an essential mediator of the sex-dependent perception of moderate cold temperatures.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Metabolic regulator ERRγ governs gastric stem cell differentiation into acid-secreting parietal cells.Cell stem cell · 2024Article
- SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Article
- Impact of KvLQT1 potassium channel modulation on alveolar fluid homeostasis in an animal model of thiourea-induced lung edema.Frontiers in physiology · 2022Article
- The Physiology of the Gastric Parietal Cell.Physiological reviews · 2020Review
- Gastric Parietal Cell Physiology and Helicobacter pylori-Induced Disease.Gastroenterology · 2019Review
- Genetic ablation of carbonic anhydrase IX disrupts gastric barrier function via claudin-18 downregulation and acid backflux.Acta physiologica (Oxford, England) · 2018Article
- Computer modeling of gastric parietal cell: significance of canalicular space, gland lumen, and variable canalicular [K+].American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Protein kinase A stimulates Kv7.1 surface expression by regulating Nedd4-2-dependent endocytic trafficking.American journal of physiology. Cell physiology · 2015Article
- Loss of Slc26a9 anion transporter alters intestinal electrolyte and HCO3(-) transport and reduces survival in CFTR-deficient mice.Pflugers Archiv : European journal of physiology · 2015Article
- Potassium channels in pancreatic duct epithelial cells: their role, function and pathophysiological relevance.Pflugers Archiv : European journal of physiology · 2015Review
- Molecular transport machinery involved in orchestrating luminal acid-induced duodenal bicarbonate secretion in vivo.The Journal of physiology · 2013Article
- How Helicobacter pylori infection controls gastric acid secretion.Journal of gastroenterology · 2012Review
- Acid secretion-associated translocation of KCNJ15 in gastric parietal cells.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Kir4.1 channel expression is essential for parietal cell control of acid secretion.The Journal of biological chemistry · 2011Article
- Selective gene expression by rat gastric corpus epithelium.Physiological genomics · 2011Article
- Update on the mechanisms of gastric acid secretion.Current gastroenterology reports · 2010Review
- Unravelling a role for KCNQ1 in K+ recycling and gastric acid secretion.The Journal of physiology · 2009Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parietal cell (PC) proton secretion via H(+)/K(+)-ATPase requires apical K(+) recycling. A variety of K(+) channels and transporters are expressed in the PC and the molecular nature of the apical K(+) recycling channel is under debate. This study was undertaken to delineate the exact function of KCNQ1 channels in gastric acid secretion. Acid secretory rates and electrophysiological parameters were determined in gastric mucosae of 7- to 8-day-old KCNQ1(+/+), (+/-) and (-/-) mice. Parietal cell ultrastructure, abundance and gene expression levels were quantified. Glandular structure and PC abundance, and housekeeping gene expression did not differ between the KCNQ1(-/-) and (+/+) mucosae. Microvillar secretory membranes were intact, but basal acid secretion was absent and forskolin-stimulated acid output reduced by approximately 90% in KCNQ1(-/-) gastric mucosa. Application of a high K(+) concentration to the luminal membrane restored normal acid secretory rates in the KCNQ1(-/-) mucosa. The study demonstrates that the KCNQ1 channel provides K(+) to the extracellular K(+) binding site of the H(+)/K(+)-ATPase during acid secretion, and no other gastric K(+) channel can substitute for this function.
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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.