ArticleJournal of molecular medicine (Berlin, Germany)2019
Plasma membrane-localized TMEM16 proteins are indispensable for expression of CFTR.
Article in Journal of molecular medicine (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Benzbromarone as adjuvant therapy for cystic fibrosis lung disease: a pilot clinical trial.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2024Trial
- Review
- Functional Interdependence of Anoctamins May Influence Conclusions from Overexpression Studies.International journal of molecular sciences · 2024Article
- The tether function of the anoctamins.Cell calcium · 2024Review
- Pathogenic Relationships in Cystic Fibrosis and Renal Diseases: CFTR, SLC26A9 and Anoctamins.International journal of molecular sciences · 2023Review
- Urinary Biomarkers in Monitoring the Progression and Treatment of Autosomal Dominant Polycystic Kidney Disease-The Promised Land?Medicina (Kaunas, Lithuania) · 2023Review
- TMEM16A/F support exocytosis but do not inhibit Notch-mediated goblet cell metaplasia of BCi-NS1.1 human airway epithelium.Frontiers in physiology · 2023Article
- Expression of SLC26A9 in Airways and Its Potential Role in Asthma.International journal of molecular sciences · 2022Article
- Paneth Cell Secretion in vivo Requires Expression of Tmem16a and Tmem16f.Gastro hep advances · 2022Article
- The chloride channel CFTR is not required for cyst growth in an ADPKD mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- CLCA1 Regulates Airway Mucus Production and Ion Secretion Through TMEM16A.International journal of molecular sciences · 2021Article
- Decoding information on COVID-19: Ontological approach towards design possible therapeutics.Informatics in medicine unlocked · 2021Review
- Transport properties in CFTR-/- knockout piglets suggest normal airway surface liquid pH and enhanced amiloride-sensitive NaPflugers Archiv : European journal of physiology · 2020Article
- Pendrin stimulates a chloride absorption pathway to increase CFTR-mediated chloride secretion from Cystic Fibrosis airway epithelia.FASEB bioAdvances · 2020Article
- Cyst growth in ADPKD is prevented by pharmacological and genetic inhibition of TMEM16A in vivo.Nature communications · 2020Article
- Pharmacological Inhibition and Activation of the CaInternational journal of molecular sciences · 2020Article
- CaFrontiers in cell and developmental biology · 2020Article
- Novel Anti-Inflammatory Approaches for Cystic Fibrosis Lung Disease: Identification of Molecular Targets and Design of Innovative Therapies.Frontiers in pharmacology · 2020Review
- TMEM16A chloride channel does not drive mucus production.Life science alliance · 2019Article
- Mucus, mucins, and cystic fibrosis.Pediatric pulmonology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cystic fibrosis transmembrane conductance regulator (CFTR) is the secretory chloride channel in epithelial tissues that has a central role in cystic fibrosis (CF) lung and gastrointestinal disease. A recent publication demonstrates a close association between CFTR and TMEM16A, the calcium-activated chloride channel. Thus, no CFTR chloride currents could be detected in airways and large intestine from mice lacking epithelial expression of TMEM16A. Here, we demonstrate that another plasma membrane-localized TMEM16 paralogue, TMEM16F, can compensate for the lack of TMEM16A. Using TMEM16 knockout mice, human lymphocytes, and a number of human cell lines with endogenous protein expression or heterologous expression, we demonstrate that CFTR can only function in the presence of either TMEM16A or TMEM16F. Double knockout of intestinal epithelial TMEM16A/F expression did not produce offsprings, suggesting a lethal phenotype in utero. Plasma membrane-localized TMEM16A or TMEM16F is required for exocytosis and expression of CFTR in the plasma membrane. TMEM16A/F proteins may therefore have an impact on disease severity in CF. KEY MESSAGES: • Cystic fibrosis is caused by the defective 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.