The normal abstract identifies BEST1/VMD2 variants associated with retinal disease. It supplies disease and membrane-protein context rather than a modern direct channel mechanism.

The normal abstract and selected full-text paragraphs distinguish human RPE surface labeling, native macaque/porcine basolateral staining and human protein expressed in rat RPE-J cells. The expressed-cell intracellular staining does not establish a soluble cytosolic pool.

The normal abstract directly identifies calcium-sensitive human bestrophin chloride currents, oligomeric behavior and dominant mutant effects after heterologous expression. It establishes channel capability rather than relying solely on disease association.

The normal abstract describes bestrophin anion-channel structure-function analysis. The human activity is independently corroborated; no claim of a complete figure or supplemental audit is made.

Normal abstract plus selected indexed primary Results/Discussion support human epithelial-cell and expressed-human-protein chloride currents, alongside separate animal epithelial observations. The early channel-versus-regulator discussion and intracellular/possibly vesicular localization are kept distinct from later human pore evidence. The normal cache remains abstract-only.

The normal abstract links biallelic human BEST1 variants to a distinct retinopathy and altered chloride currents. It supports a disease-associated channel defect without implying all recessive cases share that mechanism.

The normal abstract separately reports human BEST1 bicarbonate permeability and conductance among several bestrophin homologs. Human BEST1 is directly assayed, so its bicarbonate activity is not a paralog transfer.

Normal abstract and selected primary Results/Discussion support human BEST1 N/C-terminal interaction and multimeric channels. Functional terminal-interaction defects need not abolish oligomerization; the study does not independently fix the later established pentamer stoichiometry.

The normal cache is abstract-only; selected authenticated additional primary text was read separately and remains quarantined. Expressed wild-type BEST1 is basolateral in MDCKII cells, while particular variants alter distribution and function. The broader cache was not substituted for the protected canonical file.

The normal abstract reports wild-type/mutant human BEST1 whole-cell recordings and localization in polarized MDCKII cells. Individual panel details beyond this reading are not claimed.

The normal abstract describes human iPSC-RPE and expressed-protein studies, including preserved channel function in a particular recessive-disease variant combination. Its title is not evidence against BEST1 being an anion channel.

The normal abstract reports a human recessive-retinopathy family, wild-type/mutant HEK293T currents and plasma-membrane localization. The tested variants reduce current without a universal loss of membrane localization.

The normal abstract describes human RPE apical/basolateral surface proteomics. Official identity was checked, but publisher and repository retrieval did not yield the BEST1-specific full-text/table result. The curated basal-membrane assertion is accepted with independent localization support, not claimed as newly verified from its table.

Selected normal full-text Results and figure caption describe purified wild-type human BEST1 and BEST2 pentamers and different calcium-bound conformations. BEST1’s partially open structure must not be conflated with BEST2’s fully open conformation. No complete supplementary or image audit is claimed.

The normal abstract establishes the disease-gene association for Best macular dystrophy. It supports visual-system relevance without assigning phototransduction chemistry.

The bestrophin reaction places chloride on opposite sides of the plasma membrane; passive channel activity is not constrained to the depicted direction.

The bestrophin reaction describes bicarbonate movement from cytosol to extracellular space and supports the membrane transport context.

The broad ion-channel-transport pathway supplies pathway context; human BEST1’s specific chloride and bicarbonate activities are established independently.

Official primary abstract reports Best1-mediated glial GABA release with silencing/rescue and tonic inhibition. Mouse context is retained; the original complete figures and supplement were not inspected.

Official complete abstract distinguishes slow calcium-dependent Best1-mediated astrocytic glutamate release from fast TREK-1-mediated release and describes astrocytic microdomains. This does not by itself demonstrate endogenous human astrocyte physiology.

Selected primary Results and Figures 2/3 captions show Best1-dependent hippocampal potentiation and astrocyte-specific, rather than neuronal, recovery after cell-type-specific relief of silencing. Figure images and the complete supplement were not inspected.

Selected primary Methods, Results and Discussion report very low brain Best1 expression and no specific astroglial staining with WT/KO and positive-tissue controls. This challenges localization in those preparations, but does not directly repeat all earlier release or rescue experiments.

Official abstract and selected primary parafascicular-thalamus Results/Figure 4 describe reduced astrocytic BEST1 and tonic inhibition after conditional deletion, with unchanged neuronal signal in that selected experiment. Other brain regions are reported in the abstract; a full-paper/image audit is not claimed.

Official abstract and all five figure captions, plus the primary antibody table, support mouse cortical BEST1 at glutamatergic and GABAergic terminals with WT/KO comparisons. This provides independent presynaptic evidence, not direct human neuronal localization. Figure images were not independently reanalyzed.

Official abstract, selected primary interaction Results/Discussion/Methods and human iPSC-RPE Figure 7 Results distinguish GAD65-dependent permeation, extracellular-GABA activation and imposed-condition GABA influx. Human glutamate currents and GABA influx support permeability, not physiological flux direction in intact RPE or endogenous human glial secretion.

Selected normal Results and Figure 6 legend describe an extracellular GABA-bound human BEST1 structure, a more open neck and GABA-potentiated chloride currents in HEK293 cells at 1 micromolar intracellular calcium. Methods specify human BEST1 purification and external GABA substitutions. These support a GABA-gated chloride-channel activity under the reported assay conditions, while the relevant endogenous receptor context remains unresolved.