Solute carrier family 26 member 5 (SLC26A5)

Prestin (Solute carrier family 26 member 5; SLC26A5) is a transmembrane voltage-sensitive motor protein expressed exclusively in the basolateral plasma membrane of outer hair cells of the mammalian cochlea[6][4][1]. It converts changes in membrane potential into rapid mechanical force, driving the somatic electromotility that underpins cochlear amplification and frequency selectivity—essential for sensitive hearing in mammals[6][4][1][5]. Structurally, Prestin belongs to the SLC26/SulP family of anion exchangers, is organized as a dimer, and contains 14 transmembrane segments plus a C-terminal STAS (sulfate transporter and anti-sigma factor antagonist) domain[2][3]. Unlike related family members, Prestin serves a unique piezoelectric-like motor function rather than canonical anion transport[2][4]. Mutations in SLC26A5 are associated with nonsyndromic hearing loss (DFNB61) via impaired electromotility and OHC degeneration[1][4][5]. Prestin’s function and regulation depend on membrane cholesterol, protein interactions, intracellular calcium, and alternative splicing. No approved drugs specifically target Prestin, though its pivotal role in hearing continues to motivate therapeutic and biomarker research[1][4][6][2].

Other names

PrestinSLC26A5PRESDFNB61PRESTINSolute carrier family 26 member 5deafness, neurosensory, autosomal recessive, 61prestin (motor protein)solute carrier family 26 (anion exchanger), member 5

Ototoxic agents may block or modulate Prestin function by disturbing cholesterol interaction, cytoskeletal contacts, or anion binding. Salicylate can reduce Prestin-driven electromotility through direct interaction or possibly by modulating Prestin’s voltage dependence.