ArticleAmerican journal of physiology. Cell physiology2016
Functional assessment of SLC4A11, an integral membrane protein mutated in corneal dystrophies.
Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- High expression of the underexplored SLC4A11 protein-coding transcript is specific to the corneal endothelium.Scientific reports · 2026Article
- Sex differences in congenital hereditary endothelial dystrophy (CHED) and Slc4a11Biology of sex differences · 2026Article
- SLC4A11 is a targetable marker correlated with therapeutic responses in ovarian cancer.Journal of ovarian research · 2025Article
- Review
- Systematic review:Frontiers in medicine · 2025Review
- SLC4A11 mediates ammonia import and promotes cancer stemness in hepatocellular carcinoma.JCI insight · 2024Article
- KInternational journal of molecular sciences · 2024Article
- NHFrontiers in physiology · 2024Article
- Boric acid transport activity of marine teleost aquaporins expressed in Xenopus oocytes.Physiological reports · 2023Article
- Borate Transporters and SLC4 Bicarbonate Transporters Share Key Functional Properties.Membranes · 2023Article
- Autophagy in the normal and diseased cornea.Experimental eye research · 2022Review
- 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 HCells · 2022Review
- Boric acid transport activity of human aquaporins expressed in Xenopus oocytes.Physiological reports · 2022Article
- HumanmicroPublication biology · 2022Article
- Mutational analysis in sodium-borate cotransporter SLC4A11 in consanguineous families from Punjab, Pakistan.PloS one · 2022Article
- Altered gene expression in slc4a11Scientific reports · 2021Article
- Mitochondrial ROS Induced Lysosomal Dysfunction and Autophagy Impairment in an Animal Model of Congenital Hereditary Endothelial Dystrophy.Investigative ophthalmology & visual science · 2021Article
- Diseases of the corneal endothelium.Experimental eye research · 2021Review
- Harboyan syndrome: novel SLC4A11 mutation, clinical manifestations, and outcome of corneal transplantation.Journal of human genetics · 2021Observational
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SLC4A11, a member of the SLC4 family of bicarbonate transporters, is a widely expressed integral membrane protein, abundant in kidney and cornea. Mutations of SLC4A11 cause some cases of the blinding corneal dystrophies, congenital hereditary endothelial dystrophy, and Fuchs endothelial corneal dystrophy. These diseases are marked by fluid accumulation in the corneal stroma, secondary to defective fluid reabsorption by the corneal endothelium. The role of SLC4A11 in these corneal dystrophies is not firmly established, as SLC4A11 function remains unclear. To clarify the normal function(s) of SLC4A11, we characterized the protein following expression in the simple, low-background expression system Xenopus laevis oocytes. Since plant and fungal SLC4A11 orthologs transport borate, we measured cell swelling associated with accumulation of solute borate. The plant water/borate transporter NIP5;1 manifested borate transport, whereas human SLC4A11 did not. SLC4A11 supported osmotically driven water accumulation that was electroneutral and Na
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