The synaptic vesicle protein 2C mediates the uptake of botulinum neurotoxin A into phrenic nerves
Copyright policy )The synaptic vesicle protein 2C mediates the uptake of botulinum neurotoxin A into phrenic nerves
Botulinum neurotoxins (BoNTs) inhibit neurotransmitter release by selectively cleaving core components of the vesicular fusion machinery. The synaptic vesicle proteins Synaptotagmin‐I and ‐II act as receptors for BoNT/B and BoNT/G. Here we show that BoNT/A also interacts with a synaptic vesicle protein, the synaptic vesicle glycoprotein 2C (SV2C), but not with the homologous proteins SV2A and SV2B. Binding of BoNT/A occurs at the membrane juxtaposed region preceding transmembrane domain 8. A peptide comprising the intravesicular domain between transmembrane domains 7 and 8 specifically reduces the neurotoxicity of BoNT/A at phrenic nerve preparations demonstrating the physiological relevance of this interaction.
- MRC Laboratory of Molecular Biology United Kingdom
- Hannover Medical School Germany
- Medical Research Council United Kingdom
SV2, Membrane Glycoproteins, Recombinant Fusion Proteins, Nerve Tissue Proteins, Phrenic nerve, Protein Structure, Tertiary, Phrenic Nerve, Mice, Protein Transport, Ganglioside, Botulinum neurotoxin, Animals, Protein receptor, Botulinum Toxins, Type A, Protein Binding
SV2, Membrane Glycoproteins, Recombinant Fusion Proteins, Nerve Tissue Proteins, Phrenic nerve, Protein Structure, Tertiary, Phrenic Nerve, Mice, Protein Transport, Ganglioside, Botulinum neurotoxin, Animals, Protein receptor, Botulinum Toxins, Type A, Protein Binding
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