ArticleMolecular pharmacology2012
Gβγ inhibits exocytosis via interaction with critical residues on soluble N-ethylmaleimide-sensitive factor attachment protein-25.
Article in Molecular pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Gβγ-SNAP25 exocytotic brake removal enhances insulin action, promotes adipocyte browning, and protects against diet-induced obesity.The Journal of clinical investigation · 2023Article
- SNAP25 differentially contributes to GFrontiers in cellular neuroscience · 2023Article
- Heterosynaptic GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Disabling Gβγ-SNAP-25 interaction in gene-targeted mice results in enhancement of long-term potentiation at Schaffer collateral-CA1 synapses in the hippocampus.Neuroreport · 2019Article
- Gβγ SNARE Interactions and Their Behavioral Effects.Neurochemical research · 2019Review
- Disabling the Gβγ-SNARE interaction disrupts GPCR-mediated presynaptic inhibition, leading to physiological and behavioral phenotypes.Science signaling · 2019Article
- The in vivo specificity of synaptic Gβ and Gγ subunits to the αScientific reports · 2019Article
- The expanding roles and mechanisms of G protein-mediated presynaptic inhibition.The Journal of biological chemistry · 2019Review
- GPCR regulation of secretion.Pharmacology & therapeutics · 2018Review
- Targeting G protein-coupled receptor signalling by blocking G proteins.Nature reviews. Drug discovery · 2018Review
- Dopamine-mediated calcium channel regulation in synaptic suppression in L. stagnalis interneurons.Channels (Austin, Tex.) · 2018Article
- Quantitative Multiple-Reaction Monitoring Proteomic Analysis of Gβ and Gγ Subunits in C57Bl6/J Brain Synaptosomes.Biochemistry · 2017Article
- Gβγ directly modulates vesicle fusion by competing with synaptotagmin for binding to neuronal SNARE proteins embedded in membranes.The Journal of biological chemistry · 2017Article
- A Presynaptic Group III mGluR Recruits Gβγ/SNARE Interactions to Inhibit Synaptic Transmission by Cone Photoreceptors in the Vertebrate Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Desensitization-resistant and -sensitive GPCR-mediated inhibition of GABA release occurs by Ca2+-dependent and -independent mechanisms at a hypothalamic synapse.Journal of neurophysiology · 2016Article
- Sensory Activation of Command Cells for Locomotion and Modulatory Mechanisms: Lessons from Lampreys.Frontiers in neural circuits · 2016Review
- Gβγ Binds to the Extreme C Terminus of SNAP25 to Mediate the Action of Gi/o-Coupled G Protein-Coupled Receptors.Molecular pharmacology · 2016Article
- Differential localization of G protein βγ subunits.Biochemistry · 2014Article
- Modulation of neurotransmission by GPCRs is dependent upon the microarchitecture of the primed vesicle complex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Spatial and temporal regulation of neurotransmitter release is a complex process accomplished by the exocytotic machinery working in tandem with numerous regulatory proteins. G-protein βγ dimers regulate the core process of exocytosis by interacting with the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins soluble N-ethylmaleimide-sensitive factor attachment protein-25 (SNAP-25), syntaxin 1A, and synaptobrevin. Gβγ binding to ternary SNAREs overlaps with calcium-dependent binding of synaptotagmin, inhibiting synaptotagmin-1 binding and fusion of the synaptic vesicle. To further explore the binding sites of Gβγ on SNAP-25, peptides based on the sequence of SNAP-25 were screened for Gβγ binding. Peptides that bound Gβγ were subjected to alanine scanning mutagenesis to determine their relevance to the Gβγ-SNAP-25 interaction. Peptides from this screen were tested in protein-protein interaction assays for their ability to modulate the interaction of Gβγ with SNAP-25. A peptide from the C terminus, residues 193 to 206, significantly inhibited the interaction. In addition, Ala mutants of SNAP-25 residues from the C terminus of SNAP-25, as well as from the amino-terminal region decreased binding to Gβ₁γ₁. When SNAP-25 with eight residues mutated to alanine was assembled with syntaxin 1A, there was significantly reduced affinity of this mutated t-SNARE for Gβγ, but it still interacted with synaptotagmin-1 in a Ca²⁺ -dependent manner and reconstituted evoked exocytosis in botulinum neurotoxin E-treated neurons. However, the mutant SNAP-25 could no longer support 5-hydroxytryptamine-mediated inhibition of exocytosis.
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