GPR18, GPR55 and GPR119 C
Unless otherwise stated all data on this page refer to the human proteins. Gene information is provided for human (Hs), mouse (Mm) and rat (Rn).
Overview
GPR18, GPR55 and GPR119 (provisional nomenclature), although showing little structural similarity to CB1 and CB2 cannabinoid receptors, respond to endogenous agents analogous to the endogenous cannabinoid ligands, as well as some natural/synthetic cannabinoid receptor ligands [16]. Although there are multiple reports to indicate that GPR18, GPR55 and GPR119 can be activated in vitro by N-arachidonoylglycine, lysophosphatidylinositol and N-oleoylethanolamide, respectively, there is a lack of evidence for activation by these lipid messengers in vivo. As such, therefore, these receptors retain their orphan status.
Receptors
Targets of relevance to immunopharmacology are highlighted in blue
|
GPR18 C
Show summary »
More detailed page |
|
GPR55
C
Show summary »
More detailed page |
|
GPR119 C
Show summary »
More detailed page |
Comments
Further reading
How to cite this family page
Database page citation (select format):
Concise Guide to PHARMACOLOGY citation:
Alexander SPH, Christopoulos A, Davenport AP, Kelly E, Mathie AA, Peters JA, Veale EL, Armstrong JF, Faccenda E, Harding SD, Davies JA et al. (2023) The Concise Guide to PHARMACOLOGY 2023/24: G protein-coupled receptors. Br J Pharmacol. 180 Suppl 2:S23-S144.
This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License
GPR18 failed to respond to a variety of lipid-derived agents in an in vitro screen [21], but has been reported to be activated by Δ9-tetrahydrocannabinol [11]. GPR55 responds to AM251 and rimonabant at micromolar concentrations, compared to their nanomolar affinity as CB1 receptor antagonists/inverse agonists [16]. It has been reported that lysophosphatidylinositol acts at other sites in addition to GPR55 [20]. N-Arachidonoylserine has been suggested to act as a low efficacy agonist/antagonist at GPR18 in vitro [10]. It has also been suggested oleoyl-lysophosphatidylcholine acts, at least in part, through GPR119 [12]. Although PSN375963 and PSN632408 produce GPR119-dependent responses in heterologous expression systems, comparison with N-oleoylethanolamide-mediated responses suggests additional mechanisms of action [12].