Probably plays a role in the control of regulated secretion in neural and endocrine cells. (Microbial infection) Receptor for C.botulinum neurotoxin type A (BoNT/A, botA); the toxin probably binds via extracellular loop 4 (PubMed:16543415). (Microbial infection) Possible receptor for C.botulinum neurotoxin type D (BoNT/D, botD) (PubMed:21483489). Not a receptor for C.botulinum neurotoxin type D (BoNT/D, botD) (PubMed:21632541). (Microbial infection) Receptor for C.botulinum neurotoxin type E (BoNT/E); the toxin probably binds via extracellular loop 4 (PubMed:18815274). It probably requires glycosylation of Asn-516 (PubMed:18815274). Interacts with SYT1 in a calcium-independent manner. Forms a complex with SYT1, syntaxin-1 and SNAP25. (Microbial infection) Interacts with C.botulinum neurotoxin type A (BoNT/A, botA). (Microbial infection) Interacts with C.botulinum neurotoxin type D (BoNT/D, botD) (PubMed:21483489). No evidence for its interaction with BoNT/D has also been published (PubMed:21632541). Associated with synaptic-like microvesicles but not with insulin-containing vesicles in insulin-secreting cells of the pancreas (By similarity). Localizes to microvesicles in the pinealocytes. Localizes to the acrosome in spermatids (By similarity). Expressed in ribbon synapses of the retina (at protein level) (PubMed:12687700). Expressed in diaphragm motor nerve terminals (at protein level) (PubMed:16543415). Expressed in hippocampus neurons (at protein level) (PubMed:18815274). Expressed during synaptogenesis in the retina (at protein level). Up-regulated upon Sv2a depletion. N-glycosylated. The N-terminal cytoplasmic domain is phosphorylated by CK1. Mice display no particular phenotype (PubMed:10624962). Single knockout mice survive significantly longer than wild-type mice upon exposure to C.botulinum neurotoxin type A (BoNT/A, botA) (PubMed:16543415). Mice lacking both Sv2a and Sv2b experience severe epileptic seizures and die immediately or shortly after birth similarly to mice lacking only Sv2a (PubMed:10624962). Single knockout mice bind reduced amounts of BoNT/A than wild-type mice (PubMed:16543415). Single knockout mice are significantly more resistant to C.botulinum neurotoxin type E (BoNT/E) than wild-type mice (PubMed:18815274). In single knockout mice, synaptobrevin (VAMP, the target of C.botulinum neurotoxin type D, BoNT/D) is degraded by BoNT/D, and hippocampal neurons bind BoNT/D (PubMed:21483489). Hippocampal neurons from young mice lacking both Sv2a and Sv2b do not bind BoNT/A, nor do they take it up (PubMed:16543415, PubMed:18815274). Hippocampal neurons from young mice lacking both Sv2a and Sv2b do not bind C.botulinum neurotoxin type E (BoNT/E), nor do they take it up (PubMed:18815274). Hippocampal neurons from young mice lacking both Sv2a and Sv2b do not bind C.botulinum neurotoxin type D (BoNT/D, botD), nor do they take it up (PubMed:21483489). Hippocampal neurons from young mice lacking both Sv2a and Sv2b take up C.botulinum neurotoxin type C (BoNT/C) and C.botulinum neurotoxin type F (BonT/F, botF) normally (PubMed:21483489). Belongs to the major facilitator superfamily. The use of this protein as a coreceptor for C.botulinum type D (BoNT/D, botD) is controversial. In double SV2A/SV2B knockout mice BoNT/D does not degrade its synaptobrevin target; introducing SV2A, SV2B or SV2C restores target cleavage (PubMed:21483489). However another group does not find a convincing interaction with SV2 (PubMed:21632541).