ArticlePLoS pathogens2017
Botulinum neurotoxin C mutants reveal different effects of syntaxin or SNAP-25 proteolysis on neuromuscular transmission.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- From Molecular Cleavage to Clinical Effect: A Probabilistic Field Model of Botulinum Toxin Action.Biology · 2026Article
- Probing the properties of PTEN specific botulinum toxin type E mutants.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Embracing the Versatility of Botulinum Neurotoxins in Conventional and New Therapeutic Applications.Toxins · 2024Review
- A DARPin promotes faster onset of botulinum neurotoxin A1 action.Nature communications · 2023Article
- Facial neuromuscular junctions and brainstem nuclei are the target of tetanus neurotoxin in cephalic tetanus.JCI insight · 2023Article
- Characterization of Serotype CD Mosaic Botulinum Neurotoxin in Comparison with Serotype C and A.Toxins · 2023Article
- Hydrogen peroxide induced by nerve injury promotes axon regeneration via connective tissue growth factor.Acta neuropathologica communications · 2022Article
- Detection of VAMP Proteolysis by Tetanus and Botulinum Neurotoxin Type B In Vivo with a Cleavage-Specific Antibody.International journal of molecular sciences · 2022Article
- Latrotoxin-Induced Neuromuscular Junction Degeneration Reveals Urocortin 2 as a Critical Contributor to Motor Axon Terminal Regeneration.International journal of molecular sciences · 2022Article
- Emerging Opportunities in Human Pluripotent Stem-Cells Based Assays to Explore the Diversity of Botulinum Neurotoxins as Future Therapeutics.International journal of molecular sciences · 2021Review
- Novel Native and Engineered Botulinum Neurotoxins.Handbook of experimental pharmacology · 2021Review
- Engineering Botulinum Neurotoxins for Enhanced Therapeutic Applications and Vaccine Development.Toxins · 2020Review
- Article
- An Agonist of the CXCR4 Receptor Strongly Promotes Regeneration of Degenerated Motor Axon Terminals.Cells · 2019Article
- Botulinum and Tetanus Neurotoxins.Annual review of biochemistry · 2019Review
- A comparison of biological activity of commercially available purified native botulinum neurotoxin serotypes A1 to F1 in vitro, ex vivo, and in vivo.Pharmacology research & perspectives · 2018Article
- Article
- Variability in venom composition of European viper subspecies limits the cross-effectiveness of antivenoms.Scientific reports · 2018Article
- Review
- Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Botulinum neurotoxin serotype C (BoNT/C) is a neuroparalytic toxin associated with outbreaks of animal botulism, particularly in birds, and is the only BoNT known to cleave two different SNARE proteins, SNAP-25 and syntaxin. BoNT/C was shown to be a good substitute for BoNT/A1 in human dystonia therapy because of its long lasting effects and absence of neuromuscular damage. Two triple mutants of BoNT/C, namely BoNT/C S51T/R52N/N53P (BoNT/C α-51) and BoNT/C L200W/M221W/I226W (BoNT/C α-3W), were recently reported to selectively cleave syntaxin and have been used here to evaluate the individual contribution of SNAP-25 and syntaxin cleavage to the effect of BoNT/C in vivo. Although BoNT/C α-51 and BoNT/C α-3W toxins cleave syntaxin with similar efficiency, we unexpectedly found also cleavage of SNAP-25, although to a lesser extent than wild type BoNT/C. Interestingly, the BoNT/C mutants exhibit reduced lethality compared to wild type toxin, a result that correlated with their residual activity against SNAP-25. In spite of this, a local injection of BoNT/C α-51 persistently impairs neuromuscular junction activity. This is due to an initial phase in which SNAP-25 cleavage causes a complete blockade of neurotransmission, and to a second phase of incomplete impairment ascribable to syntaxin cleavage. Together, these results indicate that neuroparalysis of BoNT/C at the neuromuscular junction is due to SNAP-25 cleavage, while the proteolysis of syntaxin provides a substantial, but incomplete, neuromuscular impairment. In light of this evidence, we discuss a possible clinical use of BoNT/C α-51 as a botulinum neurotoxin endowed with a wide safety margin and a long lasting effect.
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