ArticleThe Journal of biological chemistry2009
Slc26a9 is inhibited by the R-region of the cystic fibrosis transmembrane conductance regulator via the STAS domain.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 87 citations in OpenAlex.
- The role of the STAS domain in SLC26A9 for chloride ion transporter function.Biophysical journal · 2024Article
- Convergent gene losses and pseudogenizations in multiple lineages of stomachless fishes.Communications biology · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- SLC26A9 in airways and intestine: secretion or absorption?Channels (Austin, Tex.) · 2023Review
- The K-Cl cotransporter-3 in the mammalian kidney.Current opinion in nephrology and hypertension · 2023Review
- SARS-CoV-2 viral entry and replication is impaired in Cystic Fibrosis airways due to ACE2 downregulation.Nature communications · 2023Article
- SLC26A9 as a Potential Modifier and Therapeutic Target in Cystic Fibrosis Lung Disease.Biomolecules · 2022Review
- Effects of Wood Smoke Constituents on Mucin Gene Expression in Mice and Human Airway Epithelial Cells and on Nasal Epithelia of Subjects with a Susceptibility Gene Variant inEnvironmental health perspectives · 2022Article
- SLC26A9 is selected for endoplasmic reticulum associated degradation (ERAD) via Hsp70-dependent targeting of the soluble STAS domain.The Biochemical journal · 2021Article
- SLC26A9 SNP rs7512462 is not associated with lung disease severity or lung function response to ivacaftor in cystic fibrosis patients with G551D-CFTR.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2021Observational
- Genetic Modifiers of Cystic Fibrosis-Related Diabetes Have Extensive Overlap With Type 2 Diabetes and Related Traits.The Journal of clinical endocrinology and metabolism · 2020Article
- Increased expression of anion transporter SLC26A9 delays diabetes onset in cystic fibrosis.The Journal of clinical investigation · 2020Article
- Structural insights into the gating mechanism of human SLC26A9 mediated by its C-terminal sequence.Cell discovery · 2020Article
- The anion transporter SLC26A9 localizes to tight junctions and is degraded by the proteasome when co-expressed with F508del-CFTR.The Journal of biological chemistry · 2019Article
- Article
- TMEM16A in Cystic Fibrosis: Activating or Inhibiting?Frontiers in pharmacology · 2019Review
- Recent advances in developing therapeutics for cystic fibrosis.Human molecular genetics · 2018Review
- Role of the SLC26A9 Chloride Channel as Disease Modifier and Potential Therapeutic Target in Cystic Fibrosis.Frontiers in pharmacology · 2018Review
- Physiological and Pathophysiological Relevance of the Anion Transporter Slc26a9 in Multiple Organs.Frontiers in physiology · 2018Review
- Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
SLC26 proteins function as anion exchangers, channels, and sensors. Previous cellular studies have shown that Slc26a3 and Slc26a6 interact with the R-region of the cystic fibrosis transmembrane conductance regulator (CFTR), (R)CFTR, via the Slc26-STAS (sulfate transporter anti-sigma) domain, resulting in mutual transport activation. We recently showed that Slc26a9 has both nCl(-)-HCO(3)(-) exchanger and Cl(-) channel function. In this study, we show that the purified STAS domain of Slc26a9 (a9STAS) binds purified (R)CFTR. When Slc26a9 and (R)CFTR fragments are co-expressed in Xenopus oocytes, both Slc26a9-mediated nCl(-)-HCO(3)(-) exchange and Cl(-) currents are almost fully inhibited. Deletion of the Slc26a9 STAS domain (a9-DeltaSTAS) virtually eliminated the Cl(-) currents with only a modest affect on nCl(-)-HCO(3)(-) exchange activity. Co-expression of a9-DeltaSTAS and the (R)CFTR fragment did not alter the residual a9-DeltaSTAS function. Replacing the Slc26a9 STAS domain with the Slc26a6 STAS domain (a6-a9-a6) does not change Slc26a9 function and is no longer inhibited by (R)CFTR. These data indicate that the Slc26a9-STAS domain, like other Slc26-STAS domains, binds CFTR in the R-region. However, unlike previously reported data, this binding interaction inhibits Slc26a9 ion transport activity. These results imply that Slc26-STAS domains may all interact with (R)CFTR but that the physiological outcome is specific to differing Slc26 proteins, allowing for dynamic and acute fine tuning of ion transport for various epithelia.
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