Mu Opioid Receptor 1 Protein (Myc-DYKDDDDK Tag)

Catalog No. ABIN2727919

This Recombinant Mu Opioid Receptor 1 protein is expressed in HEK-293 Cells.

Quick Overview for Mu Opioid Receptor 1 Protein (Myc-DYKDDDDK Tag) (ABIN2727919)

Target: Mu Opioid Receptor 1 (OPRM1) (Opioid Receptor, mu 1 (OPRM1))

Protein Type: Recombinant

Origin: Human

Source: HEK-293 Cells

Application: Antibody Production (AbP), Standard (STD)

Purity: > 80 % as determined by SDS-PAGE and Coomassie blue staining

Product Details

Purification tag / Conjugate: This Mu Opioid Receptor 1 protein is labelled with Myc-DYKDDDDK Tag.

Characteristics:

• Recombinant human OPRM1 (transcript variant MOR-1) protein expressed in HEK293 cells.
• Produced with end-sequenced ORF clone

Application Details

Application Notes: Recombinant human proteins can be used for:
Native antigens for optimized antibody production
Positive controls in ELISA and other antibody assays

Comment:

The tag is located at the C-terminal.

Restrictions: For Research Use only

Handling

Concentration: 50 μg/mL

Buffer: 25 mM Tris.HCl, pH 7.3, 100 mM glycine, 10 % glycerol.

Storage: -80 °C

Storage Comment: Store at -80°C. Thaw on ice, aliquot to individual single-use tubes, and then re-freeze immediately. Only 2-3 freeze thaw cycles are recommended.

Target Details

Target: Mu Opioid Receptor 1 (OPRM1) (Opioid Receptor, mu 1 (OPRM1))

Alternative Name: Oprm1

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. 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 extent 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 [UniProtKB/Swiss-Prot Function]

Molecular Weight: 44.6 kDa

NCBI Accession: NP_000905

Pathways: cAMP Metabolic Process, Synaptic Membrane