ReviewCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2013
Mouse models for pendrin-associated loss of cochlear and vestibular function.
Review in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Postnatal Slc26a4 gene therapy improves hearing and structural integrity in a hereditary hearing loss model.The Journal of clinical investigation · 2026Article
- Identification of known and novel genetic variants in sensorineural hearing loss: insights from whole exome sequencing in Indian families.Molecular biology reports · 2025Article
- Inhibitors of the ubiquitin‑proteasome system rescue cellular levels and ion transport function of pathogenic pendrin (SLC26A4) protein variants.International journal of molecular medicine · 2025Article
- Comparison of vestibular function in hereditary hearing loss patients with GJB2, CDH23, and SLC26A4 variants.Scientific reports · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Compound heterozygous variants of the SLC26A4 gene in a Chinese family with enlarged vestibular aqueducts.BMC medical genomics · 2022Article
- Genetic Determinants of Non-Syndromic Enlarged Vestibular Aqueduct: A Review.Audiology research · 2021Review
- Enlarged vestibular aqueduct and Mondini Malformation: audiological, clinical, radiologic and genetic features.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2021Article
- A human induced pluripotent stem cell-based modular platform to challenge sensorineural hearing loss.Stem cells (Dayton, Ohio) · 2021Review
- Congenital Deafness and Recent Advances Towards Restoring Hearing Loss.Current protocols · 2021Article
- A novel SLC26A4 splicing mutation identified in two deaf Chinese twin sisters with enlarged vestibular aqueducts.Molecular genetics & genomic medicine · 2020Article
- Progress in Modeling and Targeting Inner Ear Disorders with Pluripotent Stem Cells.Stem cell reports · 2020Review
- Evaluation of the Normal Cochlear Second Interscalar Ridge Angle and Depth on 3D T2-Weighted Images: A Tool for the Diagnosis of Scala Communis and Incomplete Partition Type II.AJNR. American journal of neuroradiology · 2018Article
- Reduction of Cellular Expression Levels Is a Common Feature of Functionally Affected Pendrin (SLC26A4) Protein Variants.Molecular medicine (Cambridge, Mass.) · 2016Article
- Extracellular Cl(-) regulates human SO4 (2-)/anion exchanger SLC26A1 by altering pH sensitivity of anion transport.Pflugers Archiv : European journal of physiology · 2016Article
- Inhibitors of pendrin anion exchange identified in a small molecule screen increase airway surface liquid volume in cystic fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- An emerging role of pendrin in health and disease.Physiological reports · 2015Article
- Novel Roles for Chloride Channels, Exchangers, and Regulators in Chronic Inflammatory Airway Diseases.Mediators of inflammation · 2015Review
- Slc26a7 chloride channel activity and localization in mouse Reissner's membrane epithelium.PloS one · 2014Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The human gene SLC26A4 and the mouse ortholog Slc26a4 code for the protein pendrin, which is an anion exchanger expressed in apical membranes of selected epithelia. In the inner ear, pendrin is expressed in the cochlea, the vestibular labyrinth and the endolymphatic sac. Loss-of-function and hypo-functional mutations cause an enlargement of the vestibular aqueduct (EVA) and sensorineural hearing loss. The relatively high prevalence of SLC26A4 mutations provides a strong imperative to develop rational interventions that delay, ameliorate or prevent pendrin-associated loss of cochlear and vestibular function. This review summarizes recent studies in mouse models that have been developed to delineate the role of pendrin in the physiology of hearing and balance and that have brought forward the concept that a temporally and spatially limited therapy may be sufficient to secure a life-time of normal hearing in children bearing mutations of SLC26A4.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.