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SHANK1 Antibody
SHANK1 Antibody, Clone S22-21
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC |
|---|---|
| Primary Accession | Q9WV48 |
| Other Accession | NP_113939.2 |
| Host | Mouse |
| Isotype | IgG1 |
| Reactivity | Human, Mouse, Rat |
| Clonality | Monoclonal |
| Description | Mouse Anti-Rat SHANK1 Monoclonal IgG1 |
| Target/Specificity | Detects ~190-220 kDa (alternative splice variants). No cross-reactivity against Shank2 or Shank3. |
| Other Names | GKAP/SAPAP interacting protein Antibody, OTTHUMP00000174437 Antibody, SH3 and multiple ankyrin repeat domains 1 Antibody, SH3 and multiple ankyrin repeat domains protein 1 Antibody, SH3/ankyrin domain gene 1 Antibody, SHAN1_HUMAN Antibody, SHANK 1 Antibody, Shank1 Antibody, Shank1a Antibody, Somatostatin receptor interacting protein Antibody, Somatostatin receptor-interacting protein Antibody, SPANK 1 Antibody, SPANK1 Antibody, SSTR interacting protein Antibody, SSTR-interacting protein Antibody, SSTRIP Antibody, Synamon Antibody |
| Clone Names | S22-21 |
| Immunogen | Fusion protein amino acids 469-691 (SH3/PDZ domains) of rat Shank1 |
| Purification | Protein G Purified |
| Storage | -20ºC |
| Storage Buffer | PBS pH7.4, 50% glycerol, 0.09% sodium azide |
| Shipping Temperature | Blue Ice or 4ºC |
| Certificate of Analysis | 1 µg/ml of SMC-329 was sufficient for detection of Shank1 in 10 µg of rat brain lysate by colorimetric immunoblot analysis using Goat anti-mouse IgG:HRP as the secondary antibody. |
| Cellular Localization | Cytoplasm | Cell Junction | Synapse | Postsynaptic Cell Membrane | Postsynaptic Density |
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Provided below are standard protocols that you may find useful for product applications.
Background
Shank proteins make up a family of scaffold proteins identified through their interaction with a variety of membrane and cytoplasmic proteins (1). Shank proteins at postsynaptic sites of excitatory synapses play roles in signal transmission into the postsynaptic neuron. Studies suggest that Shank2 is expressed in the neurons of the developing retina, and could play a role in the neuronal differentiation of the developing retina (2). Other recent studies suggest that the disruption of glutamate receptors at the Shank postsynaptic platform could contribute to the destruction of the postsynaptic density, which underlies the synaptic dysfunction and loss in Alzheimer’s disease (3).
References
1. Sheng M., and Kim E. (2000) Journal of Cell Science. 113: 1851-1856.
2. Kim J.H., et al. (2009) Exp Mol Med. 41(4): 236-242.
3. Gong Y., et al. (2009) Brain Res. 1292: 191-198.
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