Associated Papers
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
Selection of Diagnostically Significant Regions of the SLC26A4 Gene Involved in Hearing Loss.
Danilchenko VY et al.
International Journal of Molecular Sciences, 2022
36362242 (PubMed )
Supplement: ijms-23-13453-s001.zip › Table_S2.pdf
Study on the relationship between the pathogenic mutations of SLC26A4 and CT phenotypes of inner ear in patient with sensorineural hearing loss.
Wu L et al.
Bioscience Reports, 2019
Indispensable Role of Ion Channels and Transporters in the Auditory System.
Mittal R et al.
Journal of Cellular Physiology, 2017
Mapping pathogenic mutations suggests an innovative structural model for the pendrin (SLC26A4) transmembrane domain.
Bassot C et al.
Biochimie, 2017
Diagnostic Value of SLC26A4 Mutation Status in Hereditary Hearing Loss With EVA: A PRISMA-Compliant Meta-Analysis.
Lu YJ et al.
Medicine, 2015
26683941 (PubMed )
Supplement: medi-94-e2248-s002.xls › Sheet1
Mutation Spectrum of Common Deafness-Causing Genes in Patients with Non-Syndromic Deafness in the Xiamen Area, China.
Jiang Y et al.
Plos One, 2015
Molecular epidemiology and functional assessment of novel allelic variants of SLC26A4 in non-syndromic hearing loss patients with enlarged vestibular aqueduct in China.
Yuan Y et al.
Plos One, 2012
Comprehensive molecular etiology analysis of nonsyndromic hearing impairment from typical areas in China.
Yuan Y et al.
Journal of Translational Medicine, 2009
Molecular etiology of hearing impairment in Inner Mongolia: mutations in SLC26A4 gene and relevant phenotype analysis.
Dai P et al.
Journal of Translational Medicine, 2008
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