Recombinant GluR-2 Monoclonal Antibody (AN301279L)
For research use only.
| Verified Samples | Verified Samples in IHC: Mouse brain |
| Dilution | IHC 1:200-1:1000 |
| Isotype | IgG,κ |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Applications | IHC |
| Clonality | Monoclonal;Recombinant |
| Immunogen | Recombinant Human GluR-2 protein |
| Abbre | GluR-2 |
| Synonyms | GRIA, GLUR, GluA, HBGR, GluR-K, GRIA2, GLUR2, GLURB, GluA2, GluR-K2, HBGR2, AMPA 2, AMPA selective glutamate receptor 2, AMPA2, AMPA-selective glutamate receptor 2, GLUR 2, GLUR B, GluR K2, GluR-2, GluR-B, Glutamate receptor 2, Glutamate receptor ionotropic, Glutamate receptor ionotropic AMPA 2, GluR-2 |
| Swissprot | |
| Cellular Localization | Cell membrane, Multi-pass membrane protein, Endoplasmic reticulum membrane, Multi-pass membrane protein, Cell junction, synapse, postsynaptic cell membrane, Multi-pass membrane protein, Cell junction, synapse, postsynaptic density membrane, Multi-pass membrane protein, Interaction with CACNG2, CNIH2 and CNIH3 promotes cell surface expression (By similarity). Displays a somatodendritic localization and is excluded from axons in neurons (By similarity). |
| Concentration | 0.2 mg/mL |
| Buffer | PBS, 50% glycerol, 0.05% Proclin 300, 0.05% protein protectant. |
| Purification Method | Protein A |
| Research Areas | Neuroscience |
| Clone No. | B1042 |
| Conjugation | Unconjugated |
| Storage | Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles. |
| Shipping | Ice bag |
| background | Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. This gene product belongs to a family of glutamate receptors that are sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and function as ligand-activated cation channels. These channels are assembled from 4 related subunits, GRIA1-4. The subunit encoded by this gene (GRIA2) is subject to RNA editing (CAG->CGG; Q->R) within the second transmembrane domain, which is thought to render the channel impermeable to Ca(2+). Human and animal studies suggest that pre-mRNA editing is essential for brain function, and defective GRIA2 RNA editing at the Q/R site may be relevant to amyotrophic lateral sclerosis (ALS) etiology. |
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Unconjugated
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