Involved in the targeting and/or fusion of transport vesicles to their target membrane. Interacts with VAPA and VAPB. Highly expressed in the zona incerta and rostral periolivary region of the brain. Other neuroanatomical regions show negligible expression. Expressed in the retina, expression observed in the outer segments of the photoreceptors, in the outer and inner plexiform layers, and in a subset of ganglion cells. (Microbial infection) Targeted and hydrolyzed by C.botulinum neurotoxin type X (BoNT/X) which hydrolyzes the 68-Arg-|-Ala-69 bond and probably inhibits neurotransmitter release (PubMed:28770820). It remains unknown whether BoNT/X is ever produced, or what organisms it targets. Defects in Vamp1 are the cause of lethal-wasting (lew) phenotype, a mice mutant strain. The lew mutant phenotype is inherited in an autosomal recessive manner and manifests with neurological signs. Lew animals are characterized by a general lack of movement and wasting, eventually leading to death before weaning. The affected animals die near postnatal day 15 (P15). By P10, the mutants are noticeably immobile and lay on their side. Before this stage, mutants can be identified by a failure to attempt to right themselves. In earlier perinatal stages, the mutants are of normal size and difficult to discern from their normal littermates. The affected mice can move their limbs although not in any purposeful manner. No protein is detectable in homozygous mutant animals. Belongs to the synaptobrevin family.