Human Mu-Type Opioid Receptor (OPRM1) ELISA Kit | OPRM1 elisa kit

Human Mu-Type Opioid Receptor (OPRM1) ELISA Kit

Cat. Num. AAA4503794

• Gene Names: OPRM1; MOP; MOR; LMOR; MOR1; OPRM; M-OR-1
• Reactivity: Human
• Synonyms: Mu-Type Opioid Receptor (OPRM1); Human Mu-Type Opioid Receptor (OPRM1) ELISA Kit; M-OR-1; MOR-1; MOR1; Mu opiate receptor; Mu opioid receptor; MOP; hMOP; OPRM1 elisa kit

• Reactivity: Human
• Specificity: This assay has high sensitivity and excellent specificity for detection of OMD. No significant cross-reactivity or interference between OMD and analogues was observed.
• Sequence Length: 400

• Samples: Human Serum, Plasma, Tissue Homogenates Or Other Biological Fluids
• Assay Type: Quantitative Sandwich
• Detection Range: 78.1-5000pg/mL
• Sensitivity: 31.8pg/mL.
• Intra-assay Precision: Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level OMD were tested 20 times on one plate, respectively. Intra-Assay: CV<10%
• Inter-assay Precision: Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level OMD were tested on 3 different plates, 8 replicates in each plate. CV(%) = SD/meanX100. Inter-Assay: CV<12%
• Preparation and Storage: Stable for 12 months.

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for OPRM1 elisa kit

Intended Uses: The kit is a sandwich enzyme immunoassay for the in vitro quantitative measurement of OMD in human serum, plasma, tissue homogenates or other biological fluids.

Principle of the Assay: The microtiter plate provided in this kit has been pre-coated with an antibody specific to OMD. Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody preparation specific to OMD. Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain OMD, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm +/- 10nm. The concentration of OMD in the samples is then determined by comparing the O.D. of the samples to the standard curve.

NCBI and Uniprot Product Information

• NCBI GI #: 117940060
• NCBI GeneID: 4988
• NCBI Accession #: NP_000905.3
• NCBI GenBank Nucleotide #: NM_000914.4
• UniProt Accession #: P35372; Q12930; Q4VWM1; Q4VWM2; B0FXJ1; B2R9S7; B8Q1L7; B8Q1L8; B8Q1L9; E7EWZ3; G8XRH6; G8XRH8
• Molecular Weight: 43,957 Da
• NCBI Official Full Name: mu-type opioid receptor isoform MOR-1
• NCBI Official Synonym Full Names: opioid receptor mu 1
• NCBI Official Symbol: OPRM1
• NCBI Official Synonym Symbols: MOP; MOR; LMOR; MOR1; OPRM; M-OR-1
• NCBI Protein Information: mu-type opioid receptor
• UniProt Protein Name: Mu-type opioid receptor
• Protein Family: Mu-type opioid receptor
• UniProt Gene Name: OPRM1
• UniProt Synonym Gene Names: MOR1; M-OR-1; MOR-1; MOP; hMOP

NCBI Description

This gene encodes one of at least three opioid receptors in humans; the mu opioid receptor (MOR). The MOR is the principal target of endogenous opioid peptides and opioid analgesic agents such as beta-endorphin and enkephalins. The MOR also has an important role in dependence to other drugs of abuse, such as nicotine, cocaine, and alcohol via its modulation of the dopamine system. The NM_001008503.2:c.118A>G allele has been associated with opioid and alcohol addiction and variations in pain sensitivity but evidence for it having a causal role is conflicting. Multiple transcript variants encoding different isoforms have been found for this gene. Though the canonical MOR belongs to the superfamily of 7-transmembrane-spanning G-protein-coupled receptors some isoforms of this gene have only 6 transmembrane domains. [provided by RefSeq, Oct 2013]

Uniprot Description

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).