ArticleMolecular brain2017
Direct interaction with 14-3-3γ promotes surface expression of Best1 channel in astrocyte.
Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- The role of γ-aminobutyric acid and its receptor in metabolic reprogramming and tumor progression.Biochemistry and biophysics reports · 2026Review
- Astrocyte-related proteins mediate the association of YWHAG with Alzheimer's pathology and enhance its diagnostic value.Translational psychiatry · 2026Article
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Role of the YWHAG gene mutations in Developmental and Epileptic Encephalopathy.Frontiers in neuroscience · 2025Review
- Excitotoxic Storms of Ischemic Stroke: A Non-neuronal Perspective.Molecular neurobiology · 2024Review
- A simple, rapid fluorescent reporter-based method for detection of ectopic cre recombinase expression in presumed retinal cell type-targeted mouse lines.Experimental eye research · 2023Article
- Structure and Function of the Bestrophin family of calcium-activated chloride channels.Channels (Austin, Tex.) · 2021Review
- Emerging roles of 14-3-3γ in the brain disorder.BMB reports · 2020Review
- Retinal pigment epithelium polarity in health and blinding diseases.Current opinion in cell biology · 2020Review
- Chloride Channels in Astrocytes: Structure, Roles in Brain Homeostasis and Implications in Disease.International journal of molecular sciences · 2019Review
- 14-3-3γ Haploinsufficient Mice Display Hyperactive and Stress-sensitive Behaviors.Experimental neurobiology · 2019Article
- Bestrophinopathies: perspectives on clinical disease, Bestrophin-1 function and developing therapies.Therapeutic advances in ophthalmologyReview
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundBestrophin-1 (Best1) is a calcium-activated anion channel (CAAC) that is expressed broadly in mammalian tissues including the brain. We have previously reported that Best1 is expressed in hippocampal astrocytes at the distal peri-synaptic regions, called microdomains, right next to synaptic junctions, and that it disappears from the microdomains in Alzheimer's disease mouse model. Although Best1 appears to be dynamically regulated, the mechanism of its regulation and modulation is poorly understood. It has been reported that a regulatory protein, 14-3-3 affects the surface expression of numerous membrane proteins in mammalian cells.
methodsThe protein-protein interaction between Best1 and 14-3-3γ was confirmed by yeast-two hybrid assay and BiFC method. The effect of 14-3-3γ on Best1-mediated current was measured by whole-cell patch clamp technique.
resultsWe identified 14-3-3γ as novel binding partner of Best1 in astrocytes: among 7 isoforms of 14-3-3 protein, only 14-3-3γ was found to bind specifically. We determined a binding domain on the C-terminus of Best1 which is critical for an interaction with 14-3-3γ. We also revealed that interaction between Best1 and 14-3-3γ was mediated by phosphorylation of S358 in the C-terminus of Best1. We confirmed that surface expression of Best1 and Best1-mediated whole-cell current were significantly decreased after a gene-silencingof 14-3-3γ without a significant change in total Best1 expression in cultured astrocytes. Furthermore, we discovered that 14-3-3γ-shRNA reduced Best1-mediated glutamate release from hippocampal astrocyte by recording a PAR1 receptor-induced NMDA receptor-mediated current from CA1 pyramidal neurons in hippocampal slices injected with adenovirus carrying 14-3-3γ-shRNA. Finally, through a structural modeling, we found critical amino acid residues containing S358 of Best1 exhibiting binding affinities to 14-3-3γ.
conclusions14-3-3γ promotes surface expression of Best1 channel in astrocytes through direct interaction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.