Mutations of coding regions and splice sites of SLC26A4 cause Pendred syndrome and
nonsyndromic recessive hearing loss DFNB4. SLC26A4 encodes pendrin, a …

Outer hair cell elecromotility, driven by prestin, is essential for mammalian cochlear
amplification. Here, we report the cryo-EM structures of thermostabilized prestin (PresTS) …

DFNB61 is a recessively inherited nonsyndromic hearing loss caused by mutations in
SLC26A5, the gene that encodes the voltage‐driven motor protein, prestin. Prestin is …

Prestin (SLC26A5)-mediated voltage-driven elongations and contractions of sensory outer
hair cells within the organ of Corti are essential for mammalian cochlear amplification …

Abstract Pendrin (SLC26A4) is an anion exchanger expressed in the apical membranes of
selected epithelia. Pendrin ablation causes Pendred syndrome, a genetic disorder …

Abstract Pendrin (SLC26A4) is an anion exchanger that mediates bicarbonate (HCO3−)
exchange for chloride (Cl−) and is crucial for maintaining pH and salt homeostasis in the …

Mammalian SLC26 proteins are membrane-based anion transporters that belong to the
large SLC26/SulP family, and many of their variants are associated with hereditary diseases …

Screening pathogenic variants in the SLC26A4 gene is an important part of molecular
genetic testing for hearing loss (HL) since they are one of the common causes of hereditary …

ABSTRACT KCNQ4 encodes the homotetrameric voltage-dependent potassium ion channel
Kv7. 4, and is the causative gene for autosomal dominant nonsyndromic sensorineural …

Pendrin and prestin are evolutionary-conserved membrane proteins that are essential for
normal hearing. Dysfunction of these proteins results in hearing loss in humans, and …