Epithelial cell stretching and luminal acidification lead to a retarded development of stria vascularis and deafness in mice lacking pendrin.
about
SLC26A4 targeted to the endolymphatic sac rescues hearing and balance in Slc26a4 mutant mice.Progressive irreversible hearing loss is caused by stria vascularis degeneration in an Slc26a4-insufficient mouse model of large vestibular aqueduct syndromeSlc26a4-insufficiency causes fluctuating hearing loss and stria vascularis dysfunction.Sox10 expressing cells in the lateral wall of the aged mouse and human cochlea.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.Mice deficient in H+-ATPase a4 subunit have severe hearing impairment associated with enlarged endolymphatic compartments within the inner ear.Ephrin-B2 governs morphogenesis of endolymphatic sac and duct epithelia in the mouse inner ear.Mutanlallemand (mtl) and Belly Spot and Deafness (bsd) are two new mutations of Lmx1a causing severe cochlear and vestibular defects.Endolymphatic Na⁺ and K⁺ concentrations during cochlear growth and enlargement in mice lacking Slc26a4/pendrin.Hearing loss associated with enlargement of the vestibular aqueduct: mechanistic insights from clinical phenotypes, genotypes, and mouse models.Extremely discrepant mutation spectrum of SLC26A4 between Chinese patients with isolated Mondini deformity and enlarged vestibular aqueductMouse model of enlarged vestibular aqueducts defines temporal requirement of Slc26a4 expression for hearing acquisitionMouse models for pendrin-associated loss of cochlear and vestibular functionSLC26A4 mutation testing for hearing loss associated with enlargement of the vestibular aqueduct.Mechanisms of otoconia and otolith developmentA new look at electrolyte transport in the distal tubuleThe gastric H,K-ATPase in stria vascularis contributes to pH regulation of cochlear endolymph but not to K secretion.Developmental expression of solute carrier family 26A member 4 (SLC26A4/pendrin) during amelogenesis in developing rodent teethIdentification of allelic variants of pendrin (SLC26A4) with loss and gain of function.SLC26A4 mutations in patients with moderate to severe hearing lossRegulation of sodium transport in the inner ear.The role of pendrin in the development of the murine inner ear.Potential treatments for genetic hearing loss in humans: current conundrums.Molecular architecture underlying fluid absorption by the developing inner earSlc26a4 expression prevents fluctuation of hearing in a mouse model of large vestibular aqueduct syndrome.Intrafamilial phenotypic variability in families with biallelic SLC26A4 mutations.Atrophic thyroid follicles and inner ear defects reminiscent of cochlear hypothyroidism in Slc26a4-related deafness.
P2860
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P2860
Epithelial cell stretching and luminal acidification lead to a retarded development of stria vascularis and deafness in mice lacking pendrin.
description
2011 nî lūn-bûn
@nan
2011 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի մարտին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Epithelial cell stretching and ...... fness in mice lacking pendrin.
@ast
Epithelial cell stretching and ...... fness in mice lacking pendrin.
@en
type
label
Epithelial cell stretching and ...... fness in mice lacking pendrin.
@ast
Epithelial cell stretching and ...... fness in mice lacking pendrin.
@en
prefLabel
Epithelial cell stretching and ...... fness in mice lacking pendrin.
@ast
Epithelial cell stretching and ...... fness in mice lacking pendrin.
@en
P2860
P1433
P1476
Epithelial cell stretching and ...... fness in mice lacking pendrin.
@en
P2093
Hyoung-Mi Kim
Philine Wangemann
P2860
P304
P356
10.1371/JOURNAL.PONE.0017949
P407
P577
2011-03-14T00:00:00Z