ArticleBiochemistry2017
Identification of Crucial Amino Acid Residues Involved in Agonist Signaling at the GPR55 Receptor.
Article in Biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- CNR1 and CNR2 Cannabinoid Receptor Mutations in Cancer Cells.Current issues in molecular biology · 2026Article
- Mixed squaramide thioesters as phosphate group analogues for non-competitive antagonists of the phospholipid-sensing G protein-coupled receptor GPR55.RSC chemical biology · 2026Article
- Evaluating the Antitumor Potential of Cannabichromene, Cannabigerol, and Related Compounds fromInternational journal of molecular sciences · 2025Article
- Effect of Fatty Acyl Composition for Lysophosphatidylinositol on Neuroinflammatory Responses in Primary Neuronal Cultures.Journal of molecular neuroscience : MN · 2025Article
- Effect of Fatty Acyl Composition for Lysophosphatidylinositol on Neuroinflammatory Responses in Primary Neuronal Cultures.Research square · 2025Article
- Review
- Thienopyrimidine Derivatives as GPR55 Receptor Antagonists: Insight into Structure-Activity Relationship.ACS medicinal chemistry letters · 2023Article
- Lysophosphatidylcholine: Potential Target for the Treatment of Chronic Pain.International journal of molecular sciences · 2022Review
- Novel Potent and Selective Agonists of the GPR55 Receptor Based on the 3-Benzylquinolin-2(1Pharmaceuticals (Basel, Switzerland) · 2022Article
- Identification of G protein-coupled receptor 55 (GPR55) as a target of curcumin.NPJ science of food · 2022Article
- Targeting CB2 and TRPV1: Computational Approaches for the Identification of Dual Modulators.Frontiers in molecular biosciences · 2022Article
- Peptide targeting of lysophosphatidylinositol-sensing GPR55 for osteoclastogenesis tuning.Cell communication and signaling : CCS · 2021Article
- GPR6 Structural Insights: Homology Model Construction and Docking Studies.Molecules (Basel, Switzerland) · 2020Article
- Activation of GPR55 induces neuroprotection of hippocampal neurogenesis and immune responses of neural stem cells following chronic, systemic inflammation.Brain, behavior, and immunity · 2019Article
- GPR55 deficiency is associated with increased adiposity and impaired insulin signaling in peripheral metabolic tissues.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Activation of GPR55 increases neural stem cell proliferation and promotes early adult hippocampal neurogenesis.British journal of pharmacology · 2018Article
- An Update on Non-CBCannabis and cannabinoid research · 2017Review
- Methods for the Development of In Silico GPCR Models.Methods in enzymology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
GPR55 is a newly deorphanized class A G-protein-coupled receptor that has been implicated in inflammatory pain, neuropathic pain, metabolic disorder, bone development, and cancer. Few potent GPR55 ligands have been identified to date. This is largely due to an absence of information about salient features of GPR55, such as residues important for signaling and residues implicated in the GPR55 signaling cascade. The goal of this work was to identify residues that are key for the signaling of the GPR55 endogenous ligand, l-α-lysophosphatidylinositol (LPI), as well as the signaling of the GPR55 agonist, ML184 {CID 2440433, 3-[4-(2,3-dimethylphenyl)piperazine-1-carbonyl]-N,N-dimethyl-4-pyrrolidin-1-ylbenzenesulfonamide}. Serum response element (SRE) and serum response factor (SRF) luciferase assays were used as readouts for studying LPI and ML184 signaling at the GPR55 mutants. A GPR55 R* model based on the recent δ-opioid receptor (DOR) crystal structure was used to interpret the resultant mutation data. Two residues were found to be crucial for agonist signaling at GPR55, K2.60 and E3.29, suggesting that these residues form the primary interaction site for ML184 and LPI at GPR55. Y3.32F, H(170)F, and F6.55A/L mutation results suggested that these residues are part of the orthosteric binding site for ML184, while Y3.32F and H(170)F mutation results suggest that these two residues are part of the LPI binding pocket. Y3.32L, M3.36A, and F6.48A mutation results suggest the importance of a Y3.32/M3.36/F6.48 cluster in the GPR55 signaling cascade. C(10)A and C(260)A mutations suggest that these residues form a second disulfide bridge in the extracellular domain of GPR55, occluding ligand extracellular entry in the TMH1-TMH7 region of GPR55. Taken together, these results provide the first set of discrete information about GPR55 residues important for LPI and ML184 signaling and for GPR55 activation. This information should aid in the rational design of next-generation GPR55 ligands and the creation of the first high-affinity GPR55 radioligand, a tool that is sorely needed in the field.
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