ArticleMolecular biology of the cell2008
Glycosylated SV2A and SV2B mediate the entry of botulinum neurotoxin E into neurons.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
121 citing papers in PubMed, 1 synthesis or guideline pooled it, 232 citations in OpenAlex.
- Guideline
- Article
- Structural Determinants of Synaptic Vesicle Protein 2C Ligand Selectivity and Their Impact on Dopamine Release.bioRxiv : the preprint server for biology · 2026Article
- A belt-buckle checkpoint regulates the onset of botulinum neurotoxin intoxication.Nature communications · 2026Article
- Advances in Clostridial Neurotoxins: Passage of the Intestinal Barrier and Targeting of Specific Neuronal Cells.Toxins · 2026Review
- Botulinum Neurotoxins: History, Mechanism, and Applications. A Narrative Review.Journal of neurochemistry · 2025Review
- Structures of native SV2A reveal the binding mode for tetanus neurotoxin and anti-epileptic racetams.Nature communications · 2025Article
- Cryo-EM structure of the botulinum neurotoxin A/SV2B complex and its implications for translocation.Nature communications · 2025Article
- Botulinum Toxin: A Comprehensive Review of Its Molecular Architecture and Mechanistic Action.International journal of molecular sciences · 2025Review
- Control of Synaptotagmin-1 Trafficking by SV2A-Mechanism and Consequences for Presynaptic Function and Dysfunction.Journal of neurochemistry · 2025Review
- Structures of synaptic vesicle protein 2A and 2B bound to anticonvulsants.Nature structural & molecular biology · 2024Article
- Activity of botulinum neurotoxin X and its structure when shielded by a non-toxic non-hemagglutinin protein.Communications chemistry · 2024Article
- Crystal Structure of the Catalytic Domain of a Botulinum Neurotoxin Homologue fromInternational journal of molecular sciences · 2023Article
- Presynaptic targeting of botulinum neurotoxin type A requires a tripartite PSG-Syt1-SV2 plasma membrane nanocluster for synaptic vesicle entry.The EMBO journal · 2023Article
- Structural basis for botulinum neurotoxin E recognition of synaptic vesicle protein 2.Nature communications · 2023Article
- A Comprehensive Structural Analysis ofToxins · 2023Review
- Article
- Article
- Advances in Clostridial and Related Neurotoxins.International journal of molecular sciences · 2022Article
- The Epigenetic Dimension of Protein Structure Is an Intrinsic Weakness of the AlphaFold Program.Biomolecules · 2022Article
61 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Botulinum neurotoxin E (BoNT/E) can cause paralysis in humans and animals by blocking neurotransmitter release from presynaptic nerve terminals. How this toxin targets and enters neurons is not known. Here we identified two isoforms of the synaptic vesicle protein SV2, SV2A and SV2B, as the protein receptors for BoNT/E. BoNT/E failed to enter neurons cultured from SV2A/B knockout mice; entry was restored by expressing SV2A or SV2B, but not SV2C. Mice lacking SV2B displayed reduced sensitivity to BoNT/E. The fourth luminal domain of SV2A or SV2B alone, expressed in chimeric receptors by replacing the extracellular domain of the low-density lipoprotein receptor, can restore the binding and entry of BoNT/E into neurons lacking SV2A/B. Furthermore, we found disruption of a N-glycosylation site (N573Q) within the fourth luminal domain of SV2A rendered the mutant unable to mediate the entry of BoNT/E and also reduced the entry of BoNT/A. Finally, we demonstrate that BoNT/E failed to bind and enter ganglioside-deficient neurons; entry was rescued by loading exogenous gangliosides into neuronal membranes. Together, the data reported here demonstrate that glycosylated SV2A and SV2B act in conjunction with gangliosides to mediate the entry of BoNT/E into neurons.
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Registered trials
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.