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Rabbit Anti-VAMP1 Recombinant Antibody (BA0330) (CBMAB-0936CQ)


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Summary

Host Animal
Rabbit
Specificity
Human, Mouse, Rat
Clone
BA0330
Antibody Isotype
IgG
Application
WB, IHC-P, IF

Basic Information

Immunogen
Synthetic peptide from residues in Human VAMP1
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Purity
>95% as determined by analysis by SDS-PAGE
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Vesicle Associated Membrane Protein 1
Introduction
Synapotobrevins, syntaxins, and the synaptosomal-associated protein SNAP25 are the main components of a protein complex involved in the docking and/or fusion of synaptic vesicles with the presynaptic membrane. Involved in the targeting and/or fusion of transport vesicles to their target membrane.
Entrez Gene ID
Human6843
Mouse22317
Rat25624
UniProt ID
HumanP23763
MouseQ62442
RatQ63666
Alternative Names
SYB1; SPAX1; VAMP-1
Function
Involved in the targeting and/or fusion of transport vesicles to their target membrane.
Biological Process
Biological Process SNARE complex assembly Source:GO_Central1 Publication
Biological Process vesicle fusion Source:GO_Central1 Publication
Cellular Location
Isoform 1
Cytoplasmic vesicle, secretory vesicle, synaptic vesicle membrane
Synapse, synaptosome
Isoform 2
Cytoplasmic vesicle membrane
Synapse, synaptosome
Isoform 3
Mitochondrion outer membrane
Involvement in disease
Spastic ataxia 1, autosomal dominant (SPAX1):
An autosomal dominant form of spastic ataxia, a progressive neurodegenerative disorder characterized by lower-limb spasticity and generalized ataxia with dysarthria, impaired ocular movements, and gait disturbance.
Myasthenic syndrome, congenital, 25, presynaptic (CMS25):
A form of congenital myasthenic syndrome, a group of disorders characterized by failure of neuromuscular transmission, including pre-synaptic, synaptic, and post-synaptic disorders that are not of autoimmune origin. Clinical features include easy fatigability and muscle weakness. CMS25 is an autosomal recessive form characterized by hypotonia and generalized muscle weakness apparent from birth. Affected individuals have feeding difficulties and delayed motor development, usually never achieving independent ambulation. Additional variable features include eye movement abnormalities, joint contractures, and rigid spine.
Topology
Cytoplasmic: 1-96
Helical: 97-116
Vesicular: 117-118
PTM
(Microbial infection) Targeted and hydrolyzed by C.botulinum neurotoxin type B (BoNT/B, botB) which probably hydrolyzes the 78-Gln-|-Phe-79 bond and inhibits neurotransmitter release (PubMed:22289120).
(Microbial infection) Targeted and hydrolyzed by C.botulinum neurotoxin type D (BoNT/D, botD) which probably hydrolyzes the 61-Arg-|-Leu-62 bond and inhibits neurotransmitter release (PubMed:22289120).
BoNT/D has low catalytic activity on this protein due to its sequence (PubMed:22289120).
Note that humans are not known to be infected by C.botulinum type D.
(Microbial infection) Targeted and hydrolyzed by C.botulinum neurotoxin type F (BoNT/F, botF) which probably hydrolyzes the 60-Gln-|-Lys-61 bond and inhibits neurotransmitter release (PubMed:22289120).
(Microbial infection) Targeted and hydrolyzed by C.botulinum neurotoxin type X (BoNT/X) which probably hydrolyzes the 68-Arg-|-Ala-69 bond and inhibits neurotransmitter release (PubMed:29540745).
It remains unknown whether BoNT/X is ever produced, or what organisms it targets.
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For research use only. Not intended for any clinical use.

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