ArticleThe Journal of physiology2007
SLC26A9 is a Cl(-) channel regulated by the WNK kinases.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 134 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- SLC26A11 is an atypical solute carrier with dual transport-channel function mediating lysosomal sulfate transport.Nature communications · 2026Article
- Review
- Nucleotide Variant in theJournal of clinical medicine · 2026Article
- Pancreatitis: correcting CFTR expression and function as a promising effective treatment.Frontiers in physiology · 2026Review
- Selective amino acid formulation enhances anion secretion and restores function in cystic fibrosis mutations.Frontiers in pharmacology · 2025Article
- The role of the STAS domain in SLC26A9 for chloride ion transporter function.Biophysical journal · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- SLC26A9 in airways and intestine: secretion or absorption?Channels (Austin, Tex.) · 2023Review
- Pathogenic Relationships in Cystic Fibrosis and Renal Diseases: CFTR, SLC26A9 and Anoctamins.International journal of molecular sciences · 2023Review
- Structural and functional properties of the transporter SLC26A6 reveal mechanism of coupled anion exchange.eLife · 2023Article
- Prestin's fast motor kinetics is essential for mammalian cochlear amplification.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Cryo-EM structures of thermostabilized prestin provide mechanistic insights underlying outer hair cell electromotility.Nature communications · 2022Article
- WNK Inhibition Increases Surface Liquid pH and Host Defense in Cystic Fibrosis Airway Epithelia.American journal of respiratory cell and molecular biology · 2022Article
- SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Expression of SLC26A9 in Airways and Its Potential Role in Asthma.International journal of molecular sciences · 2022Article
- SLC26A9 as a Potential Modifier and Therapeutic Target in Cystic Fibrosis Lung Disease.Biomolecules · 2022Review
- Association of genetic variants of oxidative stress responsive kinase 1 (OXSR1) with asthma exacerbations in non-smoking asthmatics.BMC pulmonary medicine · 2022Article
- Review
- SLC26A9 is selected for endoplasmic reticulum associated degradation (ERAD) via Hsp70-dependent targeting of the soluble STAS domain.The Biochemical journal · 2021Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
SLC26A9 is a member of the SLC26 family of anion transporters, which is expressed at high levels in airway and gastric surface epithelial cells. The transport properties and regulation of SLC26A9, and thus its physiological function, are not known. Here we report that SLC26A9 is a highly selective Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability that is regulated by the WNK kinases. Expression in Xenopus oocytes and simultaneous measurement of membrane potential or current, intracellular pH (pH(i)) and intracellular Cl(-) (Cl(-)(i)) revealed that expression of SLC26A9 resulted in a large Cl(-) current. SLC26A9 displays a selectivity sequence of I(-) > Br(-) > NO(3)(-) > Cl(-) > Glu(-), but it conducts Br(-) > Cl(-) > I(-) > NO(3)(-) > Glu(-), with NO(3)(-) and I(-) inhibiting the Cl(-) conductance. Similarly, expression of SLC26A9 in HEK cells resulted in a large Cl(-) current. Although detectable, OH(-) and HCO(3)(-) fluxes in oocytes expressing SLC26A9 were very small. Moreover, HCO(3)(-) had no discernable effect on the Cl(-) current, the reversal potential in the presence or absence of Cl(-)(o) and, importantly, HCO(3)(-) had no effect on Cl(-) fluxes. These findings indicate that SLC26A9 is a Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability. Co-expression of SLC26A9 with the WNK kinases WNK1, WNK3 or WNK4 inhibited SLC26A9 activity, and the inhibition was independent of WNK kinase activity. Immunolocalization in oocytes and cell surface biotinylation in HEK cells indicated that the WNK-mediated inhibition of SLC26A9 activity is caused by reduced SLC26A9 surface expression. Expression of SLC26A9 in the airway and the response of the WNKs to homeostatic stress raise the possibility that SLC26A9 serves to mediate the response of the airway to stress.
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