Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mouse model of enlarged vestibular aqueducts defines temporal requirement of Slc26a4 expression for hearing acquisition.

The Journal of clinical investigation - 1 Nov 2011

Choi Byung Yoon, Kim Hyoung-Mi, Ito Taku, Lee Kyu-Yup, Li Xiangming, Monahan Kelly, Wen Yaqing, Wilson Elizabeth, Kurima Kiyoto, Saunders Thomas L, Petralia Ronald S, Wangemann Philine, Friedman Thomas B, Griffith Andrew J

Abstract excerpt

Mutations in human SLC26A4 are a common cause of hearing loss associated with enlarged vestibular aqueducts (EVA). SLC26A4 encodes pendrin, an anion-base exchanger expressed in inner ear epithelial cells that secretes HCO3- into endolymph. Studies of Slc26a4-null mice indicate that pendrin is essential for inner ear development, but have not revealed whether pendrin is specifically necessary for homeostasis....

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Anion Transport Proteins
Share to Doxycycline

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gestational Age

Share to Hearing

Share to Hearing Loss, Sensorineural

Share to Membrane Transport Proteins

Share to Sulfate Transporters

Share to Vestibular Aqueduct

Source

Open in PubMed Open full text

Identifiers

PMID: 21965328
DOI: 10.1172/JCI59353
PMCID: PMC3204851

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mouse model of enlarged vestibular aqueducts defines temporal requirement of Slc26a4 expression for hearing acquisition.PMID 21965328Read ↗

SLC26A4 targeted to the endolymphatic sac rescues hearing and balance in Slc26a4 mutant mice.Semantic proximity Read ↗

Gene therapy for hereditary hearing loss by SLC26A4 mutations in mice reveals distinct functional roles of pendrin in normal hearing.Semantic proximity Read ↗

Hearing loss associated with enlargement of the vestibular aqueduct: mechanistic insights from clinical phenotypes, genotypes, and mouse models.Semantic proximity Read ↗

CRISPR/Cas9-mediated exon skipping to restore premature translation termination in a DFNB4 mouse model.Semantic proximity Read ↗

Progressive irreversible hearing loss is caused by stria vascularis degeneration in an Slc26a4-insufficient mouse model of large vestibular aqueduct syndrome.Semantic proximity Read ↗

Loss of cochlear HCO3- secretion causes deafness via endolymphatic acidification and inhibition of Ca2+ reabsorption in a Pendred syndrome mouse model.Semantic proximity Read ↗

Developmental changes of ENaC expression and function in the inner ear of pendrin knock-out mice as a perspective on the development of endolymphatic hydrops.Semantic proximity Read ↗

Hereditary hearing loss with thyroid abnormalities.Semantic proximity Read ↗

[Current status and perspectives of the research in Pendred syndrome].Semantic proximity Read ↗

Deep Phenotyping of a Mouse Model for Hearing Instability Disorders.Semantic proximity Read ↗

Phenotypes of SLC26A4 gene mutations: Pendred syndrome and hypoacusis with enlarged vestibular aqueduct.Semantic proximity Read ↗

Expression pattern of the mouse ortholog of the Pendred’s syndrome gene ( Pds ) suggests a key role for pendrin in the inner earSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.