GluR-2 (phospho Ser880) rabbit pAb
ENT-A5616
Description
| REF | ENT-A5616 |
|---|---|
| Category | Antibody Polyclonal |
| Description | GluR-2 (phospho Ser880) rabbit pAb |
| Source | Rabbit |
| Applications | WB;IHC;IF;ELISA |
| Reactivity | Human;Mouse;Rat |
| Reactivity | Human;Mouse;Rat |
| Dilution | Western Blot: 1/500 – 1/2000. Immunohistochemistry: 1/100 – 1/300. ELISA: 1/20000. Not yet tested in other applications. |
| Immunogen | The antiserum was produced against synthesized peptide derived from human GluR2 around the phosphorylation site of Ser880. AA range:834-883 |
| Storage Stability | -20°C/1 year |
| Clonality | Polyclonal |
| Isotype | IgG |
| Concentration | 1 mg/ml |
| Observed Band KD | 99kD |
| Human Gene ID | 2891 |
| Human Swiss Prot Nº | P42262 |
| Subcellular Location | 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). . |
Other Name: GRIA2; GLUR2; Glutamate receptor 2; GluR-2; AMPA-selective glutamate receptor 2; GluR-B; GluR-K2; Glutamate receptor ionotropic; AMPA 2; GluA2
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