|Other Names||Metabotropic glutamate receptor 7, mGluR7, GRM7, GPRC1G, MGLUR7|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP1640a was selected from the C-term region of human GPRC1G . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized 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||G-protein coupled receptor for glutamate. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Signaling inhibits adenylate cyclase activity.|
|Cellular Location||Cell membrane; Multi-pass membrane protein.|
|Tissue Location||Expressed in many areas of the brain, especially in the cerebral cortex, hippocampus, and cerebellum Expression of GRM7 isoforms in non-neuronal tissues appears to be restricted to isoform 3 and isoform 4|
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L-glutamate is the major excitatory neurotransmitter in the central nervous system and activates both ionotropic and metabotropic glutamate receptors. Glutamatergic neurotransmission is involved in most aspects of normal brain function and can be perturbed in many neuropathologic conditions. The metabotropic glutamate receptors are a family of G protein-coupled receptors, that have been divided into 3 groups on the basis of sequence homology, putative signal transduction mechanisms, and pharmacologic properties. Group I includes GRM1 and GRM5 and these receptors have been shown to activate phospholipase C. Group II includes GRM2 and GRM3 while Group III includes GRM4, GRM6, GRM7 and GRM8. Group II and III receptors are linked to the inhibition of the cyclic AMP cascade but differ in their agonist selectivities. Alternative splice variants of GRM8 have been described but their full-length nature has not been determined.
Schulz, H.L., et al., Neurosci. Lett. 326(1):37-40 (2002).Flor, P.J., et al., Neuropharmacology 36(2):153-159 (1997).Makoff, A., et al., Brain Res. Mol. Brain Res. 40(1):165-170 (1996).Scherer, S.W., et al., Genomics 31(2):230-233 (1996).Okamoto, N., et al., J. Biol. Chem. 269(2):1231-1236 (1994).
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