Target name

P42866: Mu-type opioid receptor


  Protein 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. Isoform

  Database links

Uniprot primary ID P42866
GRCP SARfari Variant Name mOPRM1_1495
PDB ID 4DKL
DrugBank ID
BioGrid ID 201972
GuidetoPHARMACOLOGY ID 319
PharmGKB ID
KEGG ID mmu:18390
Entrez Gene (Gene ID) 18390
BindingDB P42866

  Model Performance Metrics

Fingerprint type Sensitivity Specificity Accuracy F1-score AUC Matthews_corrcoef Download model
FP2 fingerprints 0.92 0.74 0.83 0.85 0.88 0.67 Download
FP4 fingerprints 0.960 0.720 0.840 0.860 0.860 0.700 Download
MACCS fingerprints 0.890 0.650 0.770 0.790 0.830 0.550 Download
Daylight fingerprints 0.800 0.760 0.780 0.790 0.820 0.560 Download
ECFP2 fingerprints 0.900 0.770 0.840 0.840 0.900 0.680 Download
ECFP4 fingerprints 0.910 0.820 0.860 0.870 0.930 0.730 Download
ECFP6 fingerprints 0.890 0.850 0.870 0.870 0.940 0.740 Download

  Download datasets

Positive dataset Negative dataset


Copyright @ 2012-2015 Computational Biology & Drug Design Group,
School of Pharmaceutical Sciences, Central South University. All rights reserved.

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