Associated Papers
SLC4A11 Revisited: Isoforms, Expression, Functions, and Unresolved Questions.
Kovaleva PA et al.
Biomolecules, 2025
Antioxidant MitoQ increases viability of human corneal endothelial cells with congenital hereditary endothelial dystrophy-associated SLC4A11 mutations.
Peshkar-Kulkarni S et al.
Ophthalmic Genetics, 2025
Investigation of the functional impact of CHED- and FECD4-associated SLC4A11 mutations in human corneal endothelial cells.
Chung DD et al.
Plos One, 2024
Corneal dystrophy mutations R125H and R804H disable SLC4A11 by altering the extracellular pH dependence of the intracellular pK that governs H+(OH-) transport.
Quade BN et al.
American Journal of Physiology. Cell Physiology, 2022
pH dependence of the Slc4a11-mediated H+ conductance is influenced by intracellular lysine residues and modified by disease-linked mutations.
Quade BN et al.
American Journal of Physiology. Cell Physiology, 2020
Molecular Mechanisms of Fuchs and Congenital Hereditary Endothelial Corneal Dystrophies.
Malhotra D et al.
Reviews of Physiology, Biochemistry and Pharmacology, 2020
Human Corneal Expression of SLC4A11, a Gene Mutated in Endothelial Corneal Dystrophies.
Malhotra D et al.
Scientific Reports, 2019
R125H, W240S, C386R, and V507I SLC4A11 mutations associated with corneal endothelial dystrophy affect the transporter function but not trafficking in PS120 cells.
Li S et al.
Experimental Eye Research, 2019
Multifunctional ion transport properties of human SLC4A11: comparison of the SLC4A11-B and SLC4A11-C variants.
Kao L et al.
American Journal of Physiology. Cell Physiology, 2016
High Throughput Assay Identifies Glafenine as a Corrector for the Folding Defect in Corneal Dystrophy-Causing Mutants of SLC4A11.
Chiu AM et al.
Investigative Ophthalmology & Visual Science, 2015
Human SLC4A11-C functions as a DIDS-stimulatable H⁺(OH⁻) permeation pathway: partial correction of R109H mutant transport.
Kao L et al.
American Journal of Physiology. Cell Physiology, 2015
Select a paper to view details