Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases. - Wikidata - wikimedia - TriplyDB

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

http://www.wikidata.org/entity/Q37470604

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SLC4A11 and the Pathophysiology of Congenital Hereditary Endothelial Dystrophy Delayed onset of congenital hereditary endothelial dystrophy due to compound heterozygous SLC4A11 mutations SLC4A11 Three-Dimensional Homology Model Rationalizes Corneal Dystrophy-Causing Mutations.NBCe1 as a model carrier for understanding the structure-function properties of Na⁺ -coupled SLC4 transporters in health and disease.Human SLC4A11-C functions as a DIDS-stimulatable H⁺(OH⁻) permeation pathway: partial correction of R109H mutant transport.Increased water flux induced by an aquaporin-1/carbonic anhydrase II interaction Human SLC4A11 Is a Novel NH3/H+ Co-transporter.Comprehensive characterization of DNA methylation changes in Fuchs endothelial corneal dystrophy.Congenital Corneal Endothelial Dystrophies Resulting From Novel De Novo Mutations.The cytoplasmic domain is essential for transport function of the integral membrane transport protein SLC4A11.Bicarbonate transport in health and disease.Conditionally Immortal Slc4a11-/- Mouse Corneal Endothelial Cell Line Recapitulates Disrupted Glutaminolysis Seen in Slc4a11-/- Mouse Model.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.Aquaporin 4 as a NH3 Channel Bicarbonate transporters in corals point towards a key step in the evolution of cnidarian calcification Loss of ion transporters and increased unfolded protein response in Fuchs' dystrophy.Vps35-deficiency impairs SLC4A11 trafficking and promotes corneal dystrophy.Mouse Slc4a11 expressed in Xenopus oocytes is an ideally selective H+/OH- conductance pathway that is stimulated by rises in intracellular and extracellular pH.H(OH), H(OH), H(OH): a holiday perspective. Focus on "Mouse Slc4a11 expressed in Xenopus oocytes is an ideally selective H+/OH- conductance pathway that is stimulated by rises in intracellular and extracellular pH".High SLC4A11 expression is an independent predictor for poor overall survival in grade 3/4 serous ovarian cancer.Deficiency of Carbonic Anhydrase II Results in a Urinary Concentrating Defect.Mouse Models of SLC4-linked Disorders of HCO3- Transporter Dysfunction.Water Transport Mediated by Other Membrane Proteins.

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Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

http://www.wikidata.org/entity/Q37470604

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 27 June 2013

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

@en

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

@nl

type

label

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

@en

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

@nl

prefLabel

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

@en

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.

@nl

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Human Molecular Genetics

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Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases

@en

P2093

Eranga N Vithana

http://www.w3.org/2001/XMLSchema#string

Gonzalo L Vilas

http://www.w3.org/2001/XMLSchema#string

James D Young

http://www.w3.org/2001/XMLSchema#string

Jodhbir S Mehta

http://www.w3.org/2001/XMLSchema#string

Jun Liu

http://www.w3.org/2001/XMLSchema#string

Sampath K Loganathan

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P2860

Corneal dystrophies

Oligomerization of SLC4A11 protein and the severity of FECD and CHED2 corneal dystrophies caused by SLC4A11 mutations

NaBC1 is a ubiquitous electrogenic Na+ -coupled borate transporter essential for cellular boron homeostasis and cell growth and proliferation

Borate transporter SLC4A11 mutations cause both Harboyan syndrome and non-syndromic corneal endothelial dystrophy

WebLogo: A Sequence Logo Generator

Appearance of water channels in Xenopus oocytes expressing red cell CHIP28 protein

Transport and regulatory characteristics of the yeast bicarbonate transporter homolog Bor1p.

Arabidopsis boron transporter for xylem loading.

Cellular and molecular biology of the aquaporin water channels

Molecular identification and characterization of novel human and mouse concentrative Na+-nucleoside cotransporter proteins (hCNT3 and mCNT3) broadly selective for purine and pyrimidine nucleosides (system cib)

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4579-4590

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scholarly article

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10.1093/HMG/DDT307

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22

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2013-06-27T00:00:00Z

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243969956

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23813972

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transmembrane protein

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3889808

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