Associated Papers
Inhibitors of the ubiquitin‑proteasome system rescue cellular levels and ion transport function of pathogenic pendrin (SLC26A4) protein variants.
Bernardinelli E et al.
International Journal of Molecular Medicine, 2025
Asymmetric pendrin homodimer reveals its molecular mechanism as anion exchanger.
Liu Q et al.
Nature Communications, 2023
37230976 (PubMed )
Supplement: 41467_2023_38303_MOESM3_ESM.xlsx › Sheet1
Genetic etiology of non-syndromic hearing loss in Latin America.
Lezirovitz K et al.
Human Genetics, 2022
Mapping pathogenic mutations suggests an innovative structural model for the pendrin (SLC26A4) transmembrane domain.
Bassot C et al.
Biochimie, 2017
Reduction of Cellular Expression Levels Is a Common Feature of Functionally Affected Pendrin (SLC26A4) Protein Variants.
de Moraes VCS et al.
Molecular Medicine (cambridge, Mass.), 2016
Molecular analysis of SLC26A4 gene in patients with nonsyndromic hearing loss and EVA: identification of two novel mutations in Brazilian patients.
de Moraes VC et al.
International Journal of Pediatric Otorhinolaryngology, 2013
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