Associated Papers
SLC4A11 Revisited: Isoforms, Expression, Functions, and Unresolved Questions.
Kovaleva PA et al.
Biomolecules, 2025
40563515 (PubMed )
Supplement: biomolecules-15-00875-s001.zip › biomolecules-3667328-supplementary.xlsx › SLC4A11_cases
From Genes to Disease: Reassessing LOXHD1 and AGBL1's Contribution to Fuchs' Dystrophy.
Tsedilina TR et al.
International Journal of Molecular Sciences, 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
Whole-Exome Sequencing of 24 Spanish Families: Candidate Genes for Non-Syndromic Pediatric Keratoconus.
González-Atienza C et al.
Genes, 2023
Systematic review of SLC4A11, ZEB1, LOXHD1, and AGBL1 variants in the development of Fuchs' endothelial corneal dystrophy.
Tsedilina TR et al.
Frontiers in Medicine, 2023
Missense mutations in the sodium borate cotransporter SLC4A11 cause late-onset Fuchs corneal dystrophy.
Riazuddin SA et al.
Human Mutation, 2010
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