SLC26

SLC26 transporters constitute a conserved family of anion exchangers that mediate chloride, bicarbonate, sulfate, iodide, and related substrate transport across epithelial membranes, thereby regulating ion homeostasis and tissue-specific physiological functions^[1][2]. Mechanistically, multiple SLC26 members interact with cystic fibrosis transmembrane conductance regulator (CFTR), linking anion exchange activity to epithelial ion transport, pH regulation, and fluid balance pathways^[3][4]. Disease-associated dysfunction of SLC26 transporters has been identified in the kidney, airway, thyroid, and inner ear, where altered transporter activity affects electrolyte handling, inflammatory responses, and sensory function^[1][3][5]. Among the family members, SLC26A4 (pendrin) functions as a chloride/bicarbonate and iodide transporter and contributes to airway surface liquid regulation, blood pressure control, and thyroid hormone-related processes^[5][6]. In experimental models, genetic deletion of Slc26a4 attenuates lipopolysaccharide-induced NF-κB activation and lung injury, supporting its utility for investigating epithelial inflammation and ion transport mechanisms^[5]. Compared with related SLC26 isoforms that primarily function as epithelial anion exchangers, SLC26A5 (prestin) displays a specialized role in cochlear outer hair cells, where voltage-dependent conformational changes drive electromotility required for mammalian auditory amplification^[6]. For experimental applications, the amphiphilic anion salicylate reversibly inhibits prestin-mediated electromotility and is widely used to investigate SLC26A5-dependent hearing mechanisms^[6].