ArticlePflugers Archiv : European journal of physiology2016
Relationship between TMEM16A/anoctamin 1 and LRRC8A.
Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Exploring the selective inhibitory effects of Flavoxate and its analogues on two chloride channels and neuronal action potentials.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Cellular Adaptation to Mechanical Stress Emerges via Cell Shrinkage Triggered by Nonlinear Calcium Elevation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dystonia caused by ANO3 variants is due to attenuated CaBMC medicine · 2025Article
- The tether function of the anoctamins.Cell calcium · 2024Review
- Piezo1, the new actor in cell volume regulation.Pflugers Archiv : European journal of physiology · 2024Review
- Hormonal regulation of non-cystic fibrosis transmembrane conductance regulator ion channels in the endocervix.F&S science · 2023Article
- TMEM16A/F support exocytosis but do not inhibit Notch-mediated goblet cell metaplasia of BCi-NS1.1 human airway epithelium.Frontiers in physiology · 2023Article
- Lysosomal solute and water transport.The Journal of cell biology · 2022Review
- VI-116, A Novel Potent Inhibitor of VRAC with Minimal Effect on ANO1.International journal of molecular sciences · 2022Article
- Sphingosine-1-Phosphate Induces ATP Release via Volume-Regulated Anion Channels in Breast Cell Lines.Life (Basel, Switzerland) · 2021Article
- Flow fluorometry quantification of anion channel VRAC subunit LRRC8A at the membrane of living U937 cells.Channels (Austin, Tex.) · 2020Article
- LRRC8A is essential for hypotonicity-, but not for DAMP-induced NLRP3 inflammasome activation.eLife · 2020Article
- Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 1: Roles of VSOR/VRAC in Cell Volume Regulation, Release of Double-Edged Signals and Apoptotic/Necrotic Cell Death.Frontiers in cell and developmental biology · 2020Review
- Acid- and Volume-Sensitive Chloride Currents in Human Chondrocytes.Frontiers in cell and developmental biology · 2020Article
- CaFrontiers in cell and developmental biology · 2020Article
- The multifaceted role of TMEM16A in cancer.Cell calcium · 2019Review
- TTYH1 and TTYH2 Serve as LRRC8A-Independent Volume-Regulated Anion Channels in Cancer Cells.Cells · 2019Article
- TMEM16F/Anoctamin 6 in Ferroptotic Cell Death.Cancers · 2019Article
- Tweety-homolog (Experimental neurobiology · 2019Article
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TMEM16A/anoctamin 1/ANO1 and VRAC/LRRC8 are independent chloride channels activated either by increase in intracellular Ca(2+) or cell swelling, respectively. In previous studies, we observed overlapping properties for both types of channels. (i) TMEM16A/ANO1 and LRRC8 are inhibited by identical compounds, (ii) the volume-regulated anion channel VRAC requires compartmentalized Ca(2+) increase to be fully activated, (iii) anoctamins are activated by cell swelling, (iv) both channels have a role for apoptotic cell death, (v) both channels are possibly located in lipid rafts/caveolae like structures, and (vi) VRAC and anoctamin 1 currents are not additive when each are fully activated. In the present study, we demonstrate in different cell types that loss of LRRC8A expression not only inhibited VRAC, but also attenuated Ca(2+) activated Cl(-) currents. Moreover, expression of LRRC8A enhanced Ca(2+) activated Cl(-) currents, and both LRRC8A and ANO1 could be coimmunoprecipitated. We found that LRRC8A becomes accessible to biotinylation upon exposure to hypotonic bath solution, while membrane capacitance was not enhanced. When intracellular Ca(2+) was increased in ANO1-expressing cells, the membrane capacitance was enhanced and increased binding of FM4-64 to the membrane was observed. As this was not seen in cells lacking ANO1 expression, a role of ANO1 for exocytosis was suggested. We propose that ANO1 and LRRC8A are activated in parallel. Thus, ionomycin or purinergic stimulation will not only activate ANO1 but also LRRC8 currents. Cell swelling will not only activate LRRC8/VRAC, but also stimulate ANO1 currents by enhancing compartmentalized Ca(2+) increase and/or through swelling induced autocrine release of ATP.
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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.