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GeneBio Systems

GluR-2 (phospho Ser880) rabbit pAb

GluR-2 (phospho Ser880) rabbit pAb

SKU:ES5636

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Size: 100μL

Source:Rabbit

Applications:WB;IHC;IF;ELISA

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

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