|Other Names||Glutamate receptor ionotropic, delta-2, GluD2, GluR delta-2 subunit, GRID2, GLURD2|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP13471b was selected from the C-term region of GRID2. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Receptor for glutamate. L-glutamate acts as an excitatory neurotransmitter at many synapses in the central nervous system. The postsynaptic actions of Glu are mediated by a variety of receptors that are named according to their selective agonists. Promotes synaptogenesis and mediates the D-Serine- dependent long term depression signals and AMPA receptor endocytosis of cerebellar parallel fiber-Purkinje cell (PF-PC) synapses through the beta-NRX1-CBLN1-GRID2 triad complex (PubMed:27418511).|
|Cellular Location||Cell membrane; Multi-pass membrane protein. Cell junction, synapse, postsynaptic cell membrane; Multi-pass membrane protein|
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Provided below are standard protocols that you may find useful for product applications.
Human glutamate receptor delta-2 (GRID2) is a relativelynew member of the family of ionotropic glutamate receptors whichare the predominant excitatory neurotransmitter receptors in themammalian brain. GRID2 is a predicted 1,007 amino acid proteinthat shares 97% identity with the mouse homolog which is expressedselectively in cerebellar Purkinje cells. A point mutation inmouse GRID2, associated with the phenotype named 'lurcher', in theheterozygous state leads to ataxia resulting from selective,cell-autonomous apoptosis of cerebellar Purkinje cells duringpostnatal development. Mice homozygous for this mutation dieshortly after birth from massive loss of mid- and hindbrain neuronsduring late embryogenesis. This strongly suggests a role for GRID2in neuronal apoptotic death.
Rose, J.E., et al. Mol. Med. 16 (7-8), 247-253 (2010) :Joubert, B.R., et al. Genome Med 2 (3), 17 (2010) :Kakegawa, W., et al. J. Neurosci. 28(6):1460-1468(2008)Sonoda, T., et al. Biochem. Biophys. Res. Commun. 350(3):748-752(2006)Yap, C.C., et al. Biochem. Biophys. Res. Commun. 301(4):1122-1128(2003)
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