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Rabbit Anti-OPRM1 Polyclonal Antibody#abs135347

Rabbit Anti-OPRM1 Polyclonal Antibody#abs135347

Please note that the price provided is only for your reference. To obtain accurate pricing information, please contact our sales representative Vecent. This product is for research use only, not for use in diagnostic prodecures or in human.

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Description

Catalog-specificationDelivery timeUSD price

abs135347-100ug

1-2 Weeks

301.0

abs135347-50ug

1-2 Weeks

201.0

Please note that the price provided is only for your reference. To obtain accurate pricing information, please contact our sales representative Vecent.


Overview

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abs135347
Other names1. The human mu opioid receptor, also known as MOR-1 or MOR1, is encoded by the OPRM1 gene. It is a type of opioid receptor that plays a crucial role in mediating the effects of mu-type opioids.
2. OPRM is an abbreviation for the mu opioid receptor, which is expressed in various regions of the brain and spinal cord. It is involved in the regulation of pain, reward, and addictive behaviors.
3. The mu opiate receptor, referred to as MOR, is a key component of the body's opioid system. It binds to endogenous opioids as well as exogenous opioids, such as morphine, to produce analgesic and euphoric effects.
4. LMOR is another acronym for the mu opioid receptor, previously known as M-OR-1. This receptor is primarily expressed in neurons and is known for its involvement in the modulation of pain sensation and central nervous system functions.
5. OPRM_HUMAN represents the human version of the mu opioid receptor, which is highly conserved across species. It plays a significant role in various physiological processes, including pain perception, mood regulation, and reward pathways.
Please note that the generated content is based on the original text information but rearranged to provide a different perspective.
SourceRabbit
SpecificityThe OPRM1 Antibody is capable of identifying total OPRM1 levels that naturally occur within an organism. There is a high degree of similarity in the resulting content when compared to the original text.
Species ReactivityHuman;Mouse;Rat
AntigenOPRM1
ApplicationTo obtain optimal results for Western blotting, we suggest diluting the primary antibody at 1:500 to 1:1000. For immunohistochemistry, we recommend using a dilution of 1:50 to 1:200. For immunofluorescence, we suggest a dilution of 1:100 to 1:500. When performing ELISA assays using peptide antigens, we suggest diluting the primary antibody at 1:20000 to 1:40000. Again, for ELISA tests using peptide antigens, we recommend using a dilution of 1:20000 to 1:40000. Please note that these dilution suggestions are based on the original text information and should be carefully considered when conducting experiments.
ImmunogenA synthesized peptide.
MW48 KD
Properties

Concentration

1mg/ml

purificationSulfoLink™ Coupling Resin was utilized to purify the antiserum through peptide affinity chromatography.
ClonalityPolyclonal Antibody
Stability & StorageIt is recommended to keep the store at -20 °C for a duration of one year. To maintain the quality, it is important to prevent any repeated freeze/thaw cycles.
Storage bufferThe storage conditions for Rabbit IgG are as follows: it is stored in phosphate buffered saline with a pH of 7.4, containing 150mM NaCl, 0.02% sodium azide, and 50% glycerol. It should be kept at a temperature of -20 °C. The stability of Rabbit IgG is guaranteed for a period of 12 months starting from the date of receipt.

Target

Background

Receptor for endogenous opioids such as beta-endorphin and endomorphin. Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone (PubMed:7905839, PubMed:7957926, PubMed:7891175, PubMed:12589820, PubMed:9689128). 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 (PubMed:7905839). 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 extent to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15 (PubMed:12068084). 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 whereas morphine induces only low desensitization and endocytosis. Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties. Involved in neurogenesis. Isoform 12 couples to GNAS and is proposed to be involved in excitatory effects (PubMed:20525224). Isoform 16 and isoform 17 do not bind agonists but may act through oligomerization with binding-competent OPRM1 isoforms and reduce their ligand binding activity (PubMed:16580639).

Tissue specificityExpressed in brain. Isoform 16 and isoform 17 are detected in brain.
Posttranslational modificationPhosphorylated. Differentially phosphorylated in basal and agonist-induced conditions. Agonist-mediated phosphorylation modulates receptor internalization. Phosphorylated by GRK2 in a agonist-dependent manner. Phosphorylation at Tyr-168 requires receptor activation, is dependent on non-receptor protein tyrosine kinase Src and results in a decrease in agonist efficacy by reducing G-protein coupling efficiency. Phosphorylated on tyrosine residues; the phosphorylation is involved in agonist-induced G-protein-independent receptor down-regulation. Phosphorylation at Ser-377 is involved in G-protein-dependent but not beta-arrestin-dependent activation of the ERK pathway (By similarity).Ubiquitinated. A basal ubiquitination seems not to be related to degradation. Ubiquitination is increased upon formation of OPRM1:OPRD1 oligomers leading to proteasomal degradation; the ubiquitination is diminished by RTP4.
Celluar localizationEndoplasmic reticulum;Endosome;Golgi apparatus;Plasma Membrane;
UniPortP35372


This product is for research use only, not for use in diagnostic prodecures or in human.


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