Product Pathways - Neuroscience
Synapsin-2 (D6S9C) Rabbit mAb #85852
|85852S||100 µl ( 10 western blots )||￥3,100.00 现货查询||购买询价|
|85852||carrier free & custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-F=Immunofluorescence (Frozen),
Species predicted to react based on 100% sequence homology: Human,
Specificity / Sensitivity
Synapsin-2 (D6S9C) Rabbit mAb recognizes endogenous levels of total synapsin-2 protein
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly503 of human synapsin-2 protein.
Confocal immunofluorescent analysis of normal mouse hippocampus (left), cortex (middle), and cerebellum (right) using Synapsin-2 (D6S9C) Rabbit mAb (green). Blue pseudocolor = DRAQ5® #4084 (Fluorescent DNA dye).
Western blot analysis of extracts from mouse brain, mouse lung, and rat brain tissues using Synapsin-2 (D6S9C) Rabbit mAb (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower).
Synapsins, a group of at least five related members (synapsins Ia, Ib, IIa, IIb, and IIIa), are abundant brain proteins essential for regulating neurotransmitter release (1,2). All synapsins contain a short amino-terminal domain that is highly conserved and phosphorylated by PKA or CaM kinase I (1). Phosphorylation of the synapsin amino-terminal domain at Ser9 inhibits its binding to phospholipids and dissociates synapsins from synaptic vesicles (2).
Synapsin proteins help control release of neurotransmitters by tethering clusters of synaptic vesicles to the actin cytoskeleton at pre-synaptic terminals (3). As might be expected given the role these proteins play in neuronal cell function, mutations in the corresponding synapsin genes have been examined for association with neurological disorders. Mutations in the corresponding SYN2 gene tentatively implicate synapsin-2 in susceptibility to schizophrenia, bipolar disorder, and autism spectrum disorders (4-6).
- Greengard, P. (1987) Mol Neurobiol 1, 81-119.
- Hosaka, M. et al. (1999) Neuron 24, 377-87.
- Cesca, F. et al. (2010) Prog Neurobiol 91, 313-48.
- Saviouk, V. et al. (2007) Schizophr Res 96, 100-11.
- Cruceanu, C. et al. (2012) PLoS One 7, e32680.
- Corradi, A. et al. (2014) Hum Mol Genet 23, 90-103.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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