ArticleNature communications2024
Neurotransmitter-bound bestrophin channel structures reveal small molecule drug targeting sites for disease treatment.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- ImmatureProceedings of the National Academy of Sciences of the United States of America · 2026Article
- From BEST1 mutations to retinal regeneration: integrating stem cell-derived RPE models and gene correction strategies.Frontiers in cell and developmental biology · 2026Review
- Microstructure and transcriptomics reveal rapid light-induced visual plasticity in the non-obligate cave dweller Oreolalax rhodostigmatus (Megophryidae, Anura).BMC genomics · 2025Article
- ImmaturebioRxiv : the preprint server for biology · 2025Article
- Extracellular vesicles as biomarkers for traumatic brain injury using a 3D in vitro human brain tissue model.Scientific reports · 2025Article
- The pentameric chloride channel BEST1 is activated by extracellular GABA.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Best1 and Best2 are two members of the bestrophin family of anion channels critically involved in the prevention of retinal degeneration and maintenance of intraocular pressure, respectively. Here, we solved glutamate- and γ-aminobutyric acid (GABA)-bound Best2 structures, which delineate an intracellular glutamate binding site and an extracellular GABA binding site on Best2, respectively, identified extracellular GABA as a permeable activator of Best2, and elucidated the co-regulation of Best2 by glutamate, GABA and glutamine synthetase in vivo. We further identified multiple small molecules as activators of the bestrophin channels. Extensive analyses were carried out for a potent activator, 4-aminobenzoic acid (PABA): PABA-bound Best1 and Best2 structures are solved and illustrate the same binding site as in GABA-bound Best2; PABA treatment rescues the functional deficiency of patient-derived Best1 mutations. Together, our results demonstrate the mechanism and potential of multiple small molecule candidates as clinically applicable drugs for bestrophin-associated diseases/conditions.
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