Target name

P35372: Mu-type opioid receptor

  Protein function

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 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 whereas morphine induces only low desensitization and endocytosis. Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties. Involved in neurogenesis. Isoform

  Database links

Uniprot primary ID P35372
GRCP SARfari Variant Name hOPRM1_166
DrugBank ID DB00899 DB00956 DB00652 DB00497 DB00327 DB01433 DB00321 DB00813 DB06274 DB00913 DB01192 DB01081 DB00504 DB00854 DB06204 DB00836 DB01466 DB00611 DB00708 DB00647 DB00318 DB00704 DB00921 DB00333 DB00295 DB00802 DB00904 DB01183 DB00844 DB00514 DB01209 DB01221 DB01227 DB00454 DB06738 DB06800 DB00193 DB01452
BioGrid ID 111033
PharmGKB ID PA31945
KEGG ID hsa:4988
Entrez Gene (Gene ID) 4988
BindingDB P35372

  Model Performance Metrics

Fingerprint type Sensitivity Specificity Accuracy F1-score AUC Matthews_corrcoef Download model
FP2 fingerprints 0.81 0.71 0.76 0.77 0.83 0.52 Download
FP4 fingerprints 0.790 0.710 0.750 0.760 0.830 0.500 Download
MACCS fingerprints 0.810 0.620 0.710 0.740 0.790 0.440 Download
Daylight fingerprints 0.680 0.760 0.720 0.710 0.760 0.440 Download
ECFP2 fingerprints 0.840 0.820 0.830 0.830 0.890 0.650 Download
ECFP4 fingerprints 0.840 0.850 0.850 0.840 0.910 0.690 Download
ECFP6 fingerprints 0.810 0.860 0.830 0.830 0.900 0.670 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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