|Application ||WB, IHC-P, IF, E|
|Other Accession||P46089, 1170006|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||35010 Da|
|Application Notes||GPR3 antibody can be used for detection of GPR3 by Western blot at 1 - 2 µg/mL. Antibody can also be used for immunohistochemistry starting at 2.5 µg/mL. For immunofluorescence start at 20 µg/mL.|
|Reconstitution & Storage||GPR3 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||GPR3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Orphan receptor with constitutive G(s) signaling activity that activate cyclic AMP. Has a potential role in modulating a number of brain functions, including behavioral responses to stress (By similarity), amyloid-beta peptide generation in neurons and neurite outgrowth (By similarity). Maintains also meiotic arrest in oocytes (By similarity).|
|Cellular Location||Cell membrane; Multi-pass membrane protein.|
|Tissue Location||Expressed predominantly in the central nervous system, and at low levels in the lung, kidney, testis, ovary and eye. Highly expressed in regions of the brain implicated in the Alzheimer disease|
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Provided below are standard protocols that you may find useful for product applications.
GPR3 Antibody: GPR3, also known as ACCA, is a G-protein coupled receptor that constitutively activates adenylate cyclase and is highly expressed in the central nervous system. Overexpression of GPR3 stimulates the production of amyloid-beta peptide (Abeta), the deposition of which is one of the pathological hallmarks of Alzheimer 's disease (AD), while the ablation of GPR3 prevented the accumulation of Abeta in vitro and in an AD mouse model. This is of particular interest because of the proximity of a reported candidate Alzheimer 's disease (AD) locus, suggesting that GPR3 may be a potential therapeutic target for the treatment of AD. GPR3 has also been shown to block the proliferation of cerebellar granule cell precursors (GCP) during postnatal development by inhibiting the Shh-induced proliferation of GCP, indicating that GPR3 activation may represent one of the signals that triggers the postnatal cell cycle exit and terminal differentiation of GPCs.
Marchesse A, Docherty JM, Nguyen T, et al. Cloning of human genes encoding novel G protein-coupled receptors. Genomics1994; 23:609-18.
Eggerickx D, Denef JF, Labbe O, et al. Molecular cloning of an orphan G-protein-coupled receptor that constitutively activates adenylate cyclase. Biochem. J.1995; 309:837-43.
Thathiah A, Spittaels K, Hoffmann M, et al. The orphan G protein-coupled receptor 3 modulates amyloid-beta peptide generation in neurons. Science2009; 323:946-951.
Blacker D, Bertram L, Saunder AJ, et al. Results of a high-resolution genome screen of 437 Alzheimer’s disease families. Hum. Mol. Genet.2003; 12:23-32.
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