ArticleAmerican journal of physiology. Cell physiology2008
Bestrophin Cl- channels are highly permeable to HCO3-.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 129 citations in OpenAlex.
- Integrated Screening Cascades for Ion-Channel Drug Discovery: Linking Structure, Electrophysiology, Safety Pharmacology, and Human-Relevant Models.International journal of molecular sciences · 2026Review
- Architectural and biochemical advances in understanding microbial COThe Plant journal : for cell and molecular biology · 2026Review
- Pancreatitis: correcting CFTR expression and function as a promising effective treatment.Frontiers in physiology · 2026Review
- Bisretinoid lipofuscin, fundus autofluorescence and retinal disease.Progress in retinal and eye research · 2025Review
- A novel founder variant in BEST1 gene causing autosomal recessive bestrophinopathy.Orphanet journal of rare diseases · 2025Article
- Bestrophin-like protein 4 is involved in photosynthetic acclimation to light fluctuations in Chlamydomonas.Plant physiology · 2024Article
- GAD65 tunes the functions of Best1 as a GABA receptor and a neurotransmitter conducting channel.Nature communications · 2024Article
- Low-CO2-inducible bestrophins outside the pyrenoid sustain high photosynthetic efficacy in diatoms.Plant physiology · 2024Article
- Transportation for fuel: Thylakoid membrane bestrophin channels facilitate HCO3- transport to the pyrenoid in diatoms.Plant physiology · 2024Article
- BEST4American journal of physiology. Cell physiology · 2024Review
- Chromosome-scale assembly of the streamlined picoeukaryoteMicrobial genomics · 2024Article
- Computational Investigation of Mechanisms for pH Modulation of Human Chloride Channels.Molecules (Basel, Switzerland) · 2023Article
- Adapting from Low to High: An Update to COPlants (Basel, Switzerland) · 2023Review
- Pharmacological modulation of chloride channels as a therapeutic strategy for neurological disorders.Frontiers in physiology · 2023Review
- Elaborate Evaluation of Farnsworth Dichotomous D-15 Panel Test Can Help Differentiate between Best Vitelliform Macular Dystrophy and Autosomal Recessive Bestrophinopathy.Ophthalmic research · 2023Article
- Article
- GABA Release from Astrocytes in Health and Disease.International journal of molecular sciences · 2022Review
- Article
- Impaired Bestrophin Channel Activity in an iPSC-RPE Model of Best Vitelliform Macular Dystrophy (BVMD) from an Early Onset Patient Carrying the P77S Dominant Mutation.International journal of molecular sciences · 2022Article
- Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bestrophin-1 (Best1) is a Cl(-) channel that is linked to various retinopathies in both humans and dogs. Dysfunction of the Best1 Cl(-) channel has been proposed to cause retinopathy because of altered Cl(-) transport across the retinal pigment epithelium (RPE). In addition to Cl(-), many Cl(-) channels also transport HCO3(-). Because HCO3(-) is physiologically important in pH regulation and in fluid and ion transport across the RPE, we measured the permeability and conductance of bestrophins to HCO3(-) relative to Cl(-). Four human bestrophin homologs (hBest1, hBest2, hBest3, and hBest4) and mouse Best2 (mBest2) were expressed in HEK cells, and the relative HCO3(-) permeability (P HCO3/PCl) and conductance (G HCO3/GCl) were determined. P HCO3/PCl was calculated from the change in reversal potential (Erev) produced by replacing extracellular Cl(-) with HCO3(-). hBest1 was highly permeable to HCO3(-) (P HCO3)/PCl = approximately 0.44). hBest2, hBest4, and mBest2 had an even higher relative HCO3(-) permeability (P HCO3/PCl = 0.6-0.7). All four bestrophins had HCO3(-) conductances that were nearly the same as Cl(-) (G HCO3/GCl = 0.9-1.1). Extracellular Na+ did not affect the permeation of hBest1 to HCO3(-). At physiological HCO3(-) concentration, HCO3(-) was also highly conductive. The hBest1 disease-causing mutations Y85H, R92C, and W93C abolished both Cl(-) and HCO3(-) currents equally. The V78C mutation changed P HCO3/PCl and G HCO3/GCl of mBest2 channels. These results raise the possibility that disease-causing mutations in hBest1 produce disease by altering HCO3(-) homeostasis as well as Cl(-) transport in the retina.
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