| Literature DB >> 16543415 |
Min Dong1, Felix Yeh, William H Tepp, Camin Dean, Eric A Johnson, Roger Janz, Edwin R Chapman.
Abstract
How the widely used botulinum neurotoxin A (BoNT/A) recognizes and enters neurons is poorly understood. We found that BoNT/A enters neurons by binding to the synaptic vesicle protein SV2 (isoforms A, B, and C). Fragments of SV2 that harbor the toxin interaction domain inhibited BoNT/A from binding to neurons. BoNT/A binding to SV2A and SV2B knockout hippocampal neurons was abolished and was restored by expressing SV2A, SV2B, or SV2C. Reduction of SV2 expression in PC12 and Neuro-2a cells also inhibited entry of BoNT/A, which could be restored by expressing SV2 isoforms. Finally, mice that lacked an SV2 isoform (SV2B) displayed reduced sensitivity to BoNT/A. Thus, SV2 acts as the protein receptor for BoNT/A.Entities:
Mesh：
Substances：
Year: 2006 PMID： 16543415 DOI： 10.1126/science.1123654
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728