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

Multifunctional ion transport properties of human SLC4A11: comparison of the SLC4A11-B and SLC4A11-C variants.

American journal of physiology. Cell physiology - 1 Nov 2016

Kao Liyo, Azimov Rustam, Shao Xuesi M, Frausto Ricardo F, Abuladze Natalia, Newman Debra, Aldave Anthony J, Kurtz Ira

Abstract excerpt

Congenital hereditary endothelial dystrophy (CHED), Harboyan syndrome (CHED with progressive sensorineural deafness), and potentially a subset of individuals with late-onset Fuchs' endothelial corneal dystrophy are caused by mutations in the SLC4A11 gene that results in corneal endothelial cell abnormalities. Originally classified as a borate transporter, the function of SLC4A11 as a transport protein remains...

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 Antiporters

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Membrane

Share to Corneal Dystrophies, Hereditary

Share to Endothelium, Corneal

Share to Hearing Loss, Sensorineural

Share to HEK293 Cells

Share to Ion Transport

Source

Open in PubMed Open full text

Identifiers

PMID: 27581649
DOI: 10.1152/ajpcell.00233.2016
PMCID: PMC5130583

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

Multifunctional ion transport properties of human SLC4A11: comparison of the SLC4A11-B and SLC4A11-C variants.PMID 27581649Read ↗

SLC4A11 and the Pathophysiology of Congenital Hereditary Endothelial Dystrophy.Semantic proximity Read ↗

SLC4A11 Revisited: Isoforms, Expression, Functions and Unresolved QuestionsSemantic proximity Read ↗

Investigation of the functional impact of CHED- and FECD4-associated SLC4A11 mutations in human corneal endothelial cells.Semantic proximity Read ↗

Functional assessment of SLC4A11, an integral membrane protein mutated in corneal dystrophies.Semantic proximity Read ↗

Molecular phenotype of SLC4A11 missense mutants: Setting the stage for personalized medicine in corneal dystrophies.Semantic proximity Read ↗

Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.Semantic proximity Read ↗

The H+ Transporter SLC4A11: Roles in Metabolism, Oxidative Stress and Mitochondrial Uncoupling.Semantic proximity Read ↗

Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2)Semantic proximity Read ↗

SLC4A11 Three-Dimensional Homology Model Rationalizes Corneal Dystrophy-Causing Mutations.Semantic proximity Read ↗

Altered gene expression in slc4a11-/- mouse cornea highlights SLC4A11 roles.Semantic proximity Read ↗

Diversity of the mammalian sodium/proton exchanger SLC9 gene family.Semantic proximity Read ↗

Human SLC4A11-C functions as a DIDS-stimulatable H⁺(OH⁻) permeation pathway: partial correction of R109H mutant transport.Semantic proximity Read ↗

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