Slc26a4 expression prevents fluctuation of hearing in a mouse model of large vestibular aqueduct syndrome
Author:
Funder
NIH
Publisher
Elsevier BV
Subject
General Neuroscience
Reference20 articles.
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2. Mouse model of enlarged vestibular aqueducts defines temporal requirement of Slc26a4 expression for hearing acquisition;Choi;J Clin Investig,2011
3. Co-expression of pendrin, vacuolar H+-ATPase alpha4-subunit and carbonic anhydrase II in epithelial cells of the murine endolymphatic sac;Dou;J Histochem Cytochem,2004
4. Targeted disruption of mouse Pds provides insight about the inner-ear defects encountered in Pendred syndrome;Everett;Hum Mol Genet,2001
5. Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS);Everett;Nat Genet,1997
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2. Study of the factors related to air-bone gap in enlarged vestibular aqueduct;Acta Oto-Laryngologica;2024-01-02
3. Cochlear transcriptome analysis of an outbred mouse population (CFW);Frontiers in Cellular Neuroscience;2023-11-29
4. Quantitative analysis and correlative evaluation of video-oculography, micro-computed tomography, and histopathology in Pendrin-null mice;Neurobiology of Disease;2023-07
5. Single-cell RNA-sequencing of stria vascularis cells in the adult Slc26a4-/- mouse;BMC Medical Genomics;2023-06-15
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