Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
about
Fuchs endothelial corneal dystrophy: current perspectivesSLC4A11 and the Pathophysiology of Congenital Hereditary Endothelial DystrophySLC4A11 prevents osmotic imbalance leading to corneal endothelial dystrophy, deafness, and polyuria.Genetics of peripheral vestibular dysfunction: lessons from mutant mouse strains.The divergence, actions, roles, and relatives of sodium-coupled bicarbonate transportersImmunocytochemical distribution of WARP (von Willebrand A domain-related protein) in the inner ear.Depletion of SLC4A11 causes cell death by apoptosis in an immortalized human corneal endothelial cell line.Glutaminolysis is Essential for Energy Production and Ion Transport in Human Corneal Endothelium.Congenital hereditary endothelial dystrophy caused by SLC4A11 mutations progresses to Harboyan syndrome.The SLC4 family of bicarbonate (HCO₃⁻) transporters.Fuchs endothelial corneal dystrophyHuman SLC4A11-C functions as a DIDS-stimulatable H⁺(OH⁻) permeation pathway: partial correction of R109H mutant transport.Molecular bases of corneal endothelial dystrophies.Human SLC4A11 Is a Novel NH3/H+ Co-transporter.The genetics of Fuchs' corneal dystrophySLC4A11 is an EIPA-sensitive Na(+) permeable pHi regulator.Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.Loss of DDRGK1 modulates SOX9 ubiquitination in spondyloepimetaphyseal dysplasia.Mis-trafficking of bicarbonate transporters: implications to human diseases.Na(+) dependent acid-base transporters in the choroid plexus; insights from slc4 and slc9 gene deletion studies.Immunocytochemical localization of the translocase of the outer mitochondrial membrane (Tom20) in the human cochlea.Functional assessment of SLC4A11, an integral membrane protein mutated in corneal dystrophies.Multifunctional ion transport properties of human SLC4A11: comparison of the SLC4A11-B and SLC4A11-C variants.Corneal dystrophy-causing SLC4A11 mutants: suitability for folding-correction therapy.Vps35-deficiency impairs SLC4A11 trafficking and promotes corneal dystrophy.Dietary supplementation of boron differentially alters expression of borate transporter (NaBCl) mRNA by jejunum and kidney of growing pigs.Mouse Slc4a11 expressed in Xenopus oocytes is an ideally selective H+/OH- conductance pathway that is stimulated by rises in intracellular and extracellular pH.
P2860
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P2860
Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
description
2009 nî lūn-bûn
@nan
2009 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
@ast
Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
@en
type
label
Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
@ast
Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
@en
prefLabel
Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
@ast
Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
@en
P2093
P2860
P356
P1476
Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.
@en
P2093
Alexander Pushkin
Charles Kim
Debra Newman
Gary C Galbraith
Mark I Rosenblatt
Natalia Abuladze
Sherri M Jones
Stacey Yeh
P2860
P304
26882-26896
P356
10.1074/JBC.M109.008102
P407
P50
P577
2009-07-08T00:00:00Z