ArticleNature communications2013
Cytotoxicity of botulinum neurotoxins reveals a direct role of syntaxin 1 and SNAP-25 in neuron survival.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 105 citations in OpenAlex.
- STX1B variant-specific synaptic dysfunction is associated with network hyperexcitability in human iPSC-derived neurons.EBioMedicine · 2026Article
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- Non-Synaptic Function and Localization of Syntaxin-Binding Protein 1 in a Mouse Model of STXBP1-Related Epileptic Encephalopathy.Annals of neurology · 2026Article
- Dual functions of SNAP25 in mouse taste buds.The Journal of physiology · 2025Article
- Safety of Onabotulinumtoxin-A for Chronic Migraine During Pregnancy and Breastfeeding: A Narrative Review.Toxins · 2025Review
- The sodium leak channel NALCN is regulated by neuronal SNARE complex proteins.Science advances · 2025Article
- Equine grass sickness is associated with major abnormalities in the ultrastructure of skeletal neuromuscular junctions.Equine veterinary journal · 2025Article
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- The Fatal Role of Enterohaemorrhagic Escherichia coli Shiga Toxin-associated Extracellular Vesicles in Host Cells.Journal of microbiology (Seoul, Korea) · 2023Review
- 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
- The SNARE protein SNAP-25 is required for normal exocytosis at auditory hair cell ribbon synapses.iScience · 2022Article
- APP accumulates with presynaptic proteins around amyloid plaques: A role for presynaptic mechanisms in Alzheimer's disease?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
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- Targeted intracellular delivery of Cas13 and Cas9 nucleases using bacterial toxin-based platforms.Cell reports · 2022Article
- Bacterial AB toxins and host-microbe interactions.Advances in microbial physiology · 2022Review
- Knockin mouse models demonstrate differential contributions of synaptotagmin-1 and -2 as receptors for botulinum neurotoxins.PLoS pathogens · 2021Article
- Pathogenic STX3 variants affecting the retinal and intestinal transcripts cause an early-onset severe retinal dystrophy in microvillus inclusion disease subjects.Human genetics · 2021Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Botulinum neurotoxins (BoNT/A-G) act by blocking synaptic vesicle exocytosis. Whether BoNTs disrupt additional neuronal functions has not been addressed. Here we report that cleavage of syntaxin 1 by BoNT/C, and cleavage of SNAP-25 by BoNT/E both induce degeneration of neurons. Furthermore, although SNAP-25 cleaved by BoNT/A still supports neuron survival, it has reduced capacity to tolerate additional mutations. We demonstrate that syntaxin 1 and SNAP-25 cooperate as SNARE proteins to support neuron survival. Exogenous expression of other homologous SNARE proteins, syntaxin 2/3/4 and SNAP-23, which are resistant to BoNT/C and E in neurons, can substitute syntaxin 1/SNAP-25 and prevent toxin-induced neuron death. Finally, we find that neuronal death is due to blockage of plasma membrane recycling processes that utilize syntaxin 1/SNAP-25, independent of synaptic vesicle exocytosis. These findings establish neuronal cytotoxicity for BoNTs and reveal syntaxin 1/SNAP-25 as the ubiquitous and essential SNARE proteins mediating multiple fusion events on neuronal plasma membranes.
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