Rabbit Anti-mu Opioid Receptor (Ser375) Polyclonal Antibody
Purified Rabbit Polyclonal Antibody (Pab)
|Application ||WB, IF, IHC-P|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||44494 Da|
|Other Names||MORA; Oprm; Oprrm1; Mu-type opioid receptor; M-OR-1; MOR-1; Opioid receptor B; Oprm1; Ror-b|
|Format||0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glyce|
|Storage||Store at -20 ℃ for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 ℃.|
|Function||Receptor for endogenous opioids such as beta-endorphin and endomorphin. Agonist binding to the receptor induces coupling to an inactive GDP-bound heterotrimeric G-protein complex and subsequent exchange of GDP for GTP in the G-protein alpha subunit leading to dissociation of the G-protein complex with the free GTP-bound G-protein alpha and the G-protein beta-gamma dimer activating downstream cellular effectors. The agonist- and cell type-specific activity is predominantly coupled to pertussis toxin-sensitive G(i) and G(o) G alpha proteins, GNAI1, GNAI2, GNAI3 and GNAO1 isoforms Alpha-1 and Alpha-2, and to a lesser extend to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15. They mediate an array of downstream cellular responses, including inhibition of adenylate cyclase activity and both N-type and L-type calcium channels, activation of inward rectifying potassium channels, mitogen-activated protein kinase (MAPK), phospholipase C (PLC), phosphoinositide/protein kinase (PKC), phosphoinositide 3-kinase (PI3K) and regulation of NF-kappa-B. Also couples to adenylate cyclase stimulatory G alpha proteins. The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4. Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization. Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction. The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins. The activation of the ERK pathway occurs either in a G-protein-dependent or a beta-arrestin-dependent manner and is regulated by agonist- specific receptor phosphorylation. Acts as a class A G-protein coupled receptor (GPCR) which dissociates from beta-arrestin at or near the plasma membrane and undergoes rapid recycling. Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling. Endogenous ligands induce rapid desensitization, endocytosis and recycling. Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties. Involved in neurogenesis.|
|Cellular Location||Cell membrane; Multi-pass membrane protein.|
|Tissue Location||Brain. Is expressed in the cerebral cortex, caudate putamen, nucleus accumbens, septal nuclei, thalamus, hippocampus, and habenula. Not detected in cerebellum|
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This gene encodes one of three opioid receptors. The mu opioid receptor is the principal target of endogenous opioid peptides and opioid analgesic agents such a s beta-endorphn and enkephalins. The NM_001008503.1:c.118A>G allele had been associated with opioid and alcohol addiction and variations in pain sensitivity but evidence is conflicting. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jun 2012]
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