| Product name: |
GluR-2 rabbit pAb |
| Reactivity: |
Human;Mouse;Rat |
| Alternative Names: |
GRIA2; GLUR2; Glutamate receptor 2; GluR-2; AMPA-selective glutamate receptor 2; GluR-B; GluR-K2; Glutamate receptor ionotropic; AMPA 2; GluA2 |
| Source: |
Rabbit |
| Dilutions: |
Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. Immunofluorescence: 1/200 - 1/1000. ELISA: 1/20000. Not yet tested in other applications. |
| Immunogen: |
The antiserum was produced against synthesized peptide derived from human GluR2. AA range:834-883 |
| Storage: |
-20°C/1 year |
| Clonality: |
Polyclonal |
| Isotype: |
IgG |
| Concentration: |
1 mg/ml |
| Observed Band: |
99kD |
| GeneID: |
2891 |
| Human Swiss-Prot No: |
P42262 |
| 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). . |
| 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. Alternative splicing, resulting in transcript variants enco |
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