ArticleAmerican journal of physiology. Cell physiology2015
Human SLC4A11-C functions as a DIDS-stimulatable H⁺(OH⁻) permeation pathway: partial correction of R109H mutant transport.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- High expression of the underexplored SLC4A11 protein-coding transcript is specific to the corneal endothelium.Scientific reports · 2026Article
- Genetics of Keratoconus: A Comprehensive Review.Genes · 2025Review
- Review
- Investigation of the functional impact of CHED- and FECD4-associated SLC4A11 mutations in human corneal endothelial cells.PloS one · 2024Article
- NHFrontiers in physiology · 2024Article
- Potential Novel Role of Membrane-Associated Carbonic Anhydrases in the Kidney.International journal of molecular sciences · 2023Review
- Borate Transporters and SLC4 Bicarbonate Transporters Share Key Functional Properties.Membranes · 2023Article
- Corneal dystrophy mutations R125H and R804H disable SLC4A11 by altering the extracellular pH dependence of the intracellular pK that governs HAmerican journal of physiology. Cell physiology · 2022Article
- The molecular identity of the characean OHProtoplasma · 2022Article
- In Silico Study to Predict the Structural and Functional Consequences of SNPs on Biomarkers of Ovarian Cancer (OC) and BPA Exposure-Associated OC.International journal of molecular sciences · 2022Article
- The HCells · 2022Review
- HumanmicroPublication biology · 2022Article
- "SLC-omics" of the kidney: solute transporters along the nephron.American journal of physiology. Cell physiology · 2021Review
- pH dependence of the Slc4a11-mediated HAmerican journal of physiology. Cell physiology · 2020Article
- Energy Shortage in Human and Mouse Models of SLC4A11-Associated Corneal Endothelial Dystrophies.Investigative ophthalmology & visual science · 2020Article
- SLC4A11 function: evidence for HAmerican journal of physiology. Cell physiology · 2020Article
- Molecular Mechanisms of Fuchs and Congenital Hereditary Endothelial Corneal Dystrophies.Reviews of physiology, biochemistry and pharmacology · 2020Review
- Slc4a11 disruption causes duct cell loss and impairs NaCl reabsorption in female mouse submandibular glands.Physiological reports · 2019Article
- Ammonia sensitive SLC4A11 mitochondrial uncoupling reduces glutamine induced oxidative stress.Redox biology · 2019Article
- Human Corneal Expression of SLC4A11, a Gene Mutated in Endothelial Corneal Dystrophies.Scientific reports · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The SLC4A11 gene mutations cause a variety of genetic corneal diseases, including congenital hereditary endothelial dystrophy 2 (CHED2), Harboyan syndrome, some cases of Fuchs' endothelial dystrophy (FECD), and possibly familial keratoconus. Three NH2-terminal variants of the human SLC4A11 gene, named SLC4A11-A, -B, and -C are known. The SLC4A11-B variant has been the focus of previous studies. Both the expression of the SLC4A11-C variant in the cornea and its functional properties have not been characterized, and therefore its potential pathophysiological role in corneal diseases remains to be explored. In the present study, we demonstrate that SLC4A11-C is the predominant SLC4A11 variant expressed in human corneal endothelial mRNA and that the transporter functions as an electrogenic H(+)(OH(-)) permeation pathway. Disulfonic stilbenes, including 4,4'-diisothiocyano-2,2'-stilbenedisulfonate (DIDS), 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonate (H2DIDS), and 4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonate (SITS), which are known to bind covalently, increased SLC4A11-C-mediated H(+)(OH(-)) flux by 150-200% without having a significant effect in mock-transfected cells. Noncovalently interacting 4,4'-diaminostilbene-2,2'-disulfonate (DADS) was without effect. We tested the efficacy of DIDS on the functionally impaired R109H mutant (SLC4A11-C numbering) that causes CHED2. DIDS (1 mM) increased H(+)(OH(-)) flux through the mutant transporter by ∼40-90%. These studies provide a basis for future testing of more specific chemically modified dilsulfonic stilbenes as potential therapeutic agents to improve the functional impairment of specific SLC4A11 mutant transporters.
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