ArticlePflugers Archiv : European journal of physiology2013
Slc26a11 is prominently expressed in the brain and functions as a chloride channel: expression in Purkinje cells and stimulation of V H⁺-ATPase.
Article in Pflugers Archiv : European journal of physiology, 2013. 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, 33 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
- Revealing the Mechanism of Aroma Production Driven by High Salt Stress inFoods (Basel, Switzerland) · 2024Article
- Static Magnetic Field Stimulation Enhances Shunting Inhibition via a SLC26 Family ClThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- SLC26A11 Inhibition Reduces Oncotic Neuronal Death and Attenuates Stroke Reperfusion Injury.Molecular neurobiology · 2023Article
- Assessing the Link between Diabetic Metabolic Dysregulation and Breast Cancer Progression.International journal of molecular sciences · 2023Article
- Identification of IQGAP1 as a SLC26A4 (Pendrin)-Binding Protein in the Kidney.Frontiers in molecular biosciences · 2022Article
- Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021Review
- Insights into the Interaction of Lysosomal Amino Acid Transporters SLC38A9 and SLC36A1 Involved in mTORC1 Signaling in C2C12 Cells.Biomolecules · 2021Article
- Ablation of polyamine catabolic enzymes provokes Purkinje cell damage, neuroinflammation, and severe ataxia.Journal of neuroinflammation · 2020Article
- Article
- Expression of calcification-related ion transporters during blue mussel larval development.Ecology and evolution · 2019Article
- Importance of SLC26 Transmembrane Anion Exchangers in Sperm Post-testicular Maturation and Fertilization Potential.Frontiers in cell and developmental biology · 2019Review
- Chloride Homeostasis in Neurons With Special Emphasis on the Olivocerebellar System: Differential Roles for Transporters and Channels.Frontiers in cellular neuroscience · 2018Review
- Functional coupling of V-ATPase and CLC-5.World journal of nephrology · 2017Review
- A Biophysical Model for Cytotoxic Cell Swelling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- A pure chloride channel mutant of CLC-5 causes Dent's disease via insufficient V-ATPase activation.Pflugers Archiv : European journal of physiology · 2016Article
- The properties, functions, and pathophysiology of maxi-anion channels.Pflugers Archiv : European journal of physiology · 2016Review
- The multiple roles of pendrin in the kidney.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2015Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
SLC26A11 (human)/Slc26a11 (mouse), also known as kidney brain anion transporter (KBAT), is a member of the SLC26 anion transporter family and shows abundant mRNA expression in the brain. However, its exact cellular distribution and subcellular localization in the brain and its functional identity and possible physiological roles remain unknown. Expression and immunostaining studies demonstrated that Slc26a11 is abundantly expressed in the cerebellum, with a predominant expression in Purkinje cells. Lower expression levels were detected in hippocampus, olfactory bulb, cerebral cortex, and subcortical structures. Patch clamp studies in HEK293 cells transfected with mouse cDNA demonstrated that Slc26a11 can function as a chloride channel that is active under basal conditions and is not regulated by calcium, forskolin, or co-expression with cystic fibrosis transmembrane regulator. Single and double immunofluorescent labeling studies demonstrated the localization of vacuolar (V) H⁺-ATPase and Slc26a11 (KBAT) in the plasma membrane in Purkinje cells. Functional studies in HEK293 cells indicated that transfection with Slc26a11 stimulated acid transport via endogenous V H⁺-ATPase. We conclude that Slc26a11 (KBAT) is prominently distributed in output neurons of various subcortical and cortical structures in the central nervous system, with specific expression in Purkinje cells and that it may operate as a chloride channel regulating acid translocation by H⁺-ATPase across the plasma membrane and in intracellular compartments.
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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.