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GluR2 Polyclonal Antibody Store at -20°C

SKU: E-AB-15810-200

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GluR2 Polyclonal Antibody Store at -20°C

 

SKU # E-AB-15810
Reactivity Human,  Mouse,  Rat
Host Rabbit
Applications IHC

 

Product Details

Isotype IgG
Host Rabbit
Reactivity Human,  Mouse,  Rat
Applications IHC
Clonality Polyclonal
Immunogen Synthetic peptide of human GRIA2
Abbre GRIA2
Synonyms AMPA 2,  AMPA selective glutamate receptor 2,  AMPA-selective glutamate receptor 2,  AMPA2,  GLUR 2,  GLUR B,  GLUR2,  GLURB,  GRIA2,  GluA2,  GluR K2,  GluR-2,  GluR-B,  GluR-K2,  Glutamate receptor 2,  Glutamate receptor ionotropic,  Glutamate receptor ionotropic AMPA 2,  Gria2,  HBGR2
Swissprot
Cellular Localization Cell membrane. Endoplasmic reticulum membrane. Cell junction>synapse>postsynaptic cell membrane. Interaction with CACNG2, CNIH2 and CNIH3 promotes cell surface expression.
Concentration 0.4 mg/mL
Buffer Phosphate buffered solution, pH 7.4, containing 0.05% stabilizer and 50% glycerol.
Purification Method Affinity purification
Research Areas Cancer,  Neuroscience
Conjugation Unconjugated
Storage Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles.
Shipping The product is shipped with ice pack,upon receipt,store it immediately at the temperature recommended.

 

Related Reagents

Applications Recommended Dilution
IHC 1:100-1:300

 

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 encoding different isoforms, (including the flip and flop isoforms that vary in their signal transduction properties), has been noted for this gene.