ArticleThe Journal of physiology2007
Abolition of Ca2+-mediated intestinal anion secretion and increased stool dehydration in mice lacking the intermediate conductance Ca2+-dependent K+ channel Kcnn4.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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Who cites it
38 citing papers in PubMed, 75 citations in OpenAlex.
- Potassium Channels of the Airway Epithelium.Acta physiologica (Oxford, England) · 2026Review
- The anion exchanger slc26a3 regulates colonic mucus expansion during steady state and in response to prostaglandin EPflugers Archiv : European journal of physiology · 2024Article
- Direct-Current Electrical Field Stimulation of Patient-Derived Colorectal Cancer Cells.Biology · 2023Article
- The exocyst complex is required for the trafficking and delivery of KCa3.1 to the basolateral membrane of polarized epithelia.American journal of physiology. Cell physiology · 2023Article
- Clearance of small intestinal crypts involves goblet cell mucus secretion by intracellular granule rupture and enterocyte ion transport.Science signaling · 2022Article
- Role of SNARE Proteins in the Insertion of KCa3.1 in the Plasma Membrane of a Polarized Epithelium.Frontiers in physiology · 2022Article
- Advances in CaExperimental and therapeutic medicine · 2020Review
- Article
- Parallel intermediate conductance KAmerican journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Article
- Different functional roles for KBiology open · 2019Article
- Colonic Potassium Absorption and Secretion in Health and Disease.Comprehensive Physiology · 2018Review
- Kcnn4 is a modifier gene of intestinal cystic fibrosis preventing lethality in the Cftr-F508del mouse.Scientific reports · 2018Article
- KThe Journal of physiology · 2018Article
- Intermediate-Conductance-Ca2-Activated K Channel IKCa1 Is Upregulated and Promotes Cell Proliferation in Cervical CancerMedical science monitor basic research · 2017Article
- Modulation of Retrograde Trafficking of KCa3.1 in a Polarized Epithelium.Frontiers in physiology · 2017Article
- The calcium-activated potassium channel KCa3.1 plays a central role in the chemotactic response of mammalian neutrophils.Acta physiologica (Oxford, England) · 2016Article
- Genetic Inhibition Of The Ubiquitin Ligase Rnf5 Attenuates Phenotypes Associated To F508del Cystic Fibrosis Mutation.Scientific reports · 2015Article
- Potassium channels in pancreatic duct epithelial cells: their role, function and pathophysiological relevance.Pflugers Archiv : European journal of physiology · 2015Review
- High expression of KCa3.1 in patients with clear cell renal carcinoma predicts high metastatic risk and poor survival.PloS one · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Intestinal fluid secretion is driven by apical membrane, cystic fibrosis transmembrane conductance regulator (CFTR)-mediated efflux of Cl- that is concentrated in cells by basolateral Na(+)-K(+)-2Cl- cotransporters (NKCC1). An absolute requirement for Cl- efflux is the parallel activation of K(+) channels which maintain a membrane potential that sustains apical anion secretion. Both cAMP and Ca(2+) are intracellular signals for intestinal Cl- secretion. The K(+) channel involved in cAMP-dependent secretion has been identified as the KCNQ1-KCNE3 complex, but the identity of the K(+) channel driving Ca(2+)-activated Cl- secretion is controversial. We have now used a Kcnn4 null mouse to show that the intermediate conductance IK1 K(+) channel is necessary and sufficient to support Ca(2+)-dependent Cl- secretion in large and small intestine. Ussing chambers were used to monitor transepithelial potential, resistance and equivalent short-circuit current in colon and jejunum from control and Kcnn4 null mice. Na(+), K(+) and water content of stools was also measured. Distal colon and small intestinal epithelia from Kcnn4 null mice had normal cAMP-dependent Cl- secretory responses. In contrast, they completely lacked Cl- secretion in response to Ca(2+)-mobilizing agonists. Ca(2+)-activated electrogenic K(+) secretion was increased in colon epithelium of mice deficient in the IK1 channel. Na(+) and water content of stools was diminished in IK1-null animals. The use of Kcnn4 null mice has allowed us to demonstrate that IK1 K(+) channels are solely responsible for driving intestinal Ca(2+)-activated Cl- secretion. The absence of this channel leads to a marked reduction in water content in the stools, probably as a consequence of decreased electrolyte and water secretion.
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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.