GluR-2 (Phospho-Tyr876) rabbit pAb
ENT-A13238
Description
| REF | ENT-A13238 |
|---|---|
| Category | Antibody Polyclonal |
| Description | GluR-2 (Phospho-Tyr876) rabbit pAb |
| Source | Rabbit |
| Applications | IHC;IF;WB |
| Reactivity | Human; Mouse; Rat |
| Reactivity | Human; Mouse; Rat |
| Dilution | IHC-p 1:50-200, WB 1:500-2000 |
| Immunogen | Synthesized peptide derived from human GluR-2 (Phospho-Tyr876) |
| 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: 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