ArticleThe Journal of physiology2010
TMEM16A/anoctamin 1 protein mediates calcium-activated chloride currents in pulmonary arterial smooth muscle cells.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 175 citations in OpenAlex.
- Genetic Determinants of Pulmonary Artery Size in over 50,000 Subjects with and without COPD.medRxiv : the preprint server for health sciences · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- TMEM16A channel signalling microdomains in the regulation of vascular function.The Journal of physiology · 2026Review
- TMEM16A in gastrointestinal and vascular smooth muscle contractility.The Journal of physiology · 2025Review
- Calcium-activated chloride channel TMEM16A opens via pi-helical transition in transmembrane segment 4.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ANO1: central role and clinical significance in non-neoplastic and neoplastic diseases.Frontiers in immunology · 2025Review
- Distinct modulation of calcium-activated chloride channel TMEM16A by drug-binding sites.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The role of anoctamin 1 in liver disease.Journal of cellular and molecular medicine · 2024Review
- Nernst-Planck-Gaussian finite element modelling of CaFrontiers in physiology · 2024Article
- Rare variants in ANO1, encoding a calcium-activated chloride channel, predispose to moyamoya disease.Brain : a journal of neurology · 2023Article
- Feedback contributions to excitation-contraction coupling in native functioning striated muscle.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- ANO10 Function in Health and Disease.Cerebellum (London, England) · 2023Review
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Phosphatidylinositol 4,5-Bisphosphate and Cholesterol Regulators of the Calcium-Activated Chloride Channels TMEM16A and TMEM16B.Advances in experimental medicine and biology · 2023Article
- Acute oxygen sensing by vascular smooth muscle cells.Frontiers in physiology · 2023Review
- Article
- Role of Ion Channel Remodeling in Endothelial Dysfunction Induced by Pulmonary Arterial Hypertension.Biomolecules · 2022Review
- Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022Review
- Molecular mechanisms of activation and regulation of ANO1-Encoded CaChannels (Austin, Tex.) · 2021Review
- Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Calcium-activated chloride channels (CaCCs) play important roles in several physiological processes. In vascular smooth muscle, activation of these ion channels by agonist-induced Ca(2+) release results in membrane depolarization and vasoconstriction. The molecular identity of vascular CaCCs is not fully defined. Here we present evidence that TMEM16A (or anoctamin 1), a member of the transmembrane 16 (TMEM16) protein family, forms CaCCs in pulmonary artery smooth muscle cells (PASMCs). Patch-clamp analysis in freshly isolated PASMCs revealed strongly outward-rectifying, slowly activating Ca(2+)-activated Cl(-) currents sharing a high degree of similarity with heterologous TMEM16A currents. TMEM16A mRNA was identified in rat and human pulmonary arteries and various other vascular smooth muscle cell types. Further analyses revealed that several TMEM16A splice variants were detected in rat PASMCs and that TMEM16F and TMEM16K were also expressed in these cells, while TMEM16B, TMEM16D and TMEM16E were all at least 50 times less abundantly expressed and the remaining TMEM16 family members were absent. Downregulation of TMEM16A gene expression in primary cultures of rat PASMCs, with small interfering RNAs, was accompanied by almost total loss of whole-cell CaCC currents. Based on these results, we propose that TMEM16A is the major constituent of the vascular calcium-activated chloride channel in rat pulmonary artery smooth muscle.
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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.