ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Differential abilities of SNAP-25 homologs to support neuronal function.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- The Association of SNAP25 Gene Polymorphisms in Attention Deficit/Hyperactivity Disorder: a Systematic Review and Meta-Analysis.Molecular neurobiology · 2017Pooled it
- SNAP-25 disease variants affect synaptic transmission by destabilizing SNARE complexes within a multimeric SNARE ring.Cell reports · 2026Article
- Adenylyl Cyclases as Therapeutic Targets in Neuroregeneration.International journal of molecular sciences · 2025Review
- The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Integrative mRNA and miRNA Expression Profiles from Developing Zebrafish Head Highlight Brain-Preference Genes and Regulatory Networks.Molecular neurobiology · 2025Article
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- Munc13- and SNAP25-dependent molecular bridges play a key role in synaptic vesicle priming.Science advances · 2023Article
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- An Atypical, Staged Cell Death Pathway Induced by Depletion of SNARE-Proteins MUNC18-1 or Syntaxin-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Faithful SM proteins chaperone SNAREs on path to successful assembly.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Genetic disorders of neurotransmitter release machinery.Frontiers in synaptic neuroscience · 2023Review
- The SNARE protein SNAP-25 is required for normal exocytosis at auditory hair cell ribbon synapses.iScience · 2022Article
- A dynamic template complex mediates Munc18-chaperoned SNARE assembly.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The role of snare proteins in cortical development.Developmental neurobiology · 2022Review
- Alpha-Synuclein is Involved in DYT1 Dystonia Striatal Synaptic Dysfunction.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- The mesoscale organization of syntaxin 1A and SNAP25 is determined by SNARE-SNARE interactions.eLife · 2021Article
- The RNA-Binding Protein HuD Regulates Alternative Splicing and Alternative Polyadenylation in the Mouse Neocortex.Molecules (Basel, Switzerland) · 2021Article
- Loss of MUNC18-1 leads to retrograde transport defects in neurons.Journal of neurochemistry · 2021Article
- Genes associated with cognitive performance in the Morris water maze: an RNA-seq study.Scientific reports · 2020Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The SNAP receptor (SNARE) complex, consisting of synaptosome-associated protein of 25 kDa (SNAP-25), synaptobrevin-2, and syntaxin-1, is involved in synaptic vesicles exocytosis. In addition, SNAP-25 has been implicated in constitutive exocytosis processes required for neurite outgrowth. However, at least three isoforms of SNAP-25 have been reported from neurons: SNAP-23, which is also present in non-neuronal cells, and the two alternative splice variants SNAP-25a and SNAP-25b. Here, we studied the differential ability of these isoforms to support the functions previously broadly ascribed to "SNAP-25." We studied the rescue of snap-25 null neurons in culture with different SNAP-25 homologs. We find that deletion of SNAP-25 leads to strongly reduced neuron survival, and, in the few surviving cells, impaired arborization, reduced spontaneous release, and complete arrest of evoked release. Lentiviral expression of SNAP-25a, SNAP-25b, or SNAP-23 rescued neuronal survival, arborization, amplitude, and frequency of spontaneous events. Also evoked release was rescued by all isoforms, but synchronous release required SNAP-25a/b in both glutamatergic and GABAergic neurons. SNAP-23 supported asynchronous release only, reminiscent of synaptotagmin-1 null neurons. SNAP-25b was superior to SNAP-25a in vesicle priming, resembling the shift to larger releasable vesicle pools that accompanies synaptic maturation. These data demonstrate a differential ability of SNAP-25b, SNAP-25a, and SNAP-23 to support neuronal function.
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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.