ArticleExperimental & molecular medicine2019
Anoctamin 1/TMEM16A controls intestinal Cl
Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 25 citations in OpenAlex.
- Noncanonical calcium-independent TRPM4 activation governs intestinal fluid homeostasis.Nature communications · 2026Article
- Blockade of calcium-activated chloride channel ANO1 ameliorates ionizing radiation-induced intestinal injury.Journal of advanced research · 2026Article
- Identification and pharmacological characterization of a natural folipastatin as a CFTR inhibitor and potential anti-secretory agent in a human colonoid model.BMC complementary medicine and therapies · 2025Article
- Enhanced Spatial Mapping of Mouse Gastric Muscle Layers Using a Modified Swiss Roll Technique.Journal of visualized experiments : JoVE · 2025Article
- EMC3 is critical for CFTR function and calcium mobilization in the mouse intestinal epithelium.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Mechanism of action and therapeutic value of anoctamin-1 in gastrointestinal cancers.Frontiers in immunology · 2025Review
- Live Calcium Imaging of Virus-Infected Human Intestinal Organoid Monolayers Using Genetically Encoded Calcium Indicators.Journal of visualized experiments : JoVE · 2024Article
- The Anion Channel TMEM16a/Ano1 Modulates CFTR Activity, but Does Not Function as an Apical Anion Channel in Colonic Epithelium from Cystic Fibrosis Patients and Healthy Individuals.International journal of molecular sciences · 2023Article
- ANO10 is a potential prognostic biomarker and correlates with immune infiltration in breast cancer.American journal of cancer research · 2023Article
- Effects of Milk-Derived Extracellular Vesicles on the Colonic Transcriptome and Proteome in Murine Model.Nutrients · 2022Article
- The diverse roles of TMEM16A CaJournal of advanced research · 2021Review
- Intestinal TMEM16A control luminal chloride secretion in a NHERF1 dependent manner.Biochemistry and biophysics reports · 2021Article
- Pharmacological Modulation of Ion Channels for the Treatment of Cystic Fibrosis.Journal of experimental pharmacology · 2021Review
- Lysophosphatidic Acid Increases Maturation of Brush Borders and SGLT1 Activity in MYO5B-deficient Mice, a Model of Microvillus Inclusion Disease.Gastroenterology · 2020Article
- Expression of ClEuropean archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2020Article
- Effects and interaction of dietary electrolyte balance and citric acid on the intestinal function of weaned piglets.Journal of animal science · 2020Article
- Calcium-Activated Chloride Channel ANO1/TMEM16A: Regulation of Expression and Signaling.Frontiers in physiology · 2020Review
- Control of Ion Transport by Tmem16a Expressed in Murine Intestine.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
Abstract
Calcium-activated chloride channels (CaCCs) mediate numerous physiological functions and are best known for the transport of electrolytes and water in epithelia. In the intestine, CaCC currents are considered necessary for the secretion of fluid to protect the intestinal epithelium. Although genetic ablation of ANO1/TMEM16A, a gene encoding a CaCC, reduces the carbachol-induced secretion of intestinal fluid, its mechanism of action is still unknown. Here, we confirm that ANO1 is essential for the secretion of intestinal fluid. Carbachol-induced transepithelial currents were reduced in the proximal colon of Ano1-deficient mice. Surprisingly, cholera toxin-induced and cAMP-induced fluid secretion, believed to be mediated by CFTR, were also significantly reduced in the intestine of Ano1-deficient mice. ANO1 is largely expressed in the apical membranes of intestines, as predicted for CaCCs. The Ano1-deficient colons became edematous under basal conditions and had a greater susceptibility to dextran sodium sulfate-induced colitis. However, Ano1 depletion failed to affect tumor development in a model of colorectal cancer. We thus conclude that ANO1 is necessary for cAMP- and carbachol-induced Cl
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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.