ArticleMolecular pharmacology2009
Dual role of the second extracellular loop of the cannabinoid receptor 1: ligand binding and receptor localization.
Article in Molecular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 68 citations in OpenAlex.
- Article
- Using In Silico Molecular Docking to Explain Differences in Receptor Binding Behavior of HHC and THCV Isomers: Revealing New Binding Modes.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Subtle Structural Modification of a Synthetic Cannabinoid Receptor Agonist Drastically Increases its Efficacy at the CB1 Receptor.ACS chemical neuroscience · 2023Article
- Evaluating Allosteric Perturbations in Cannabinoid Receptor 1 byACS omega · 2022Article
- Molecular Targets of Cannabinoids Associated with Depression.Current medicinal chemistry · 2022Review
- Protein Interactors and Trafficking Pathways That Regulate the Cannabinoid Type 1 Receptor (CB1R).Frontiers in molecular neuroscience · 2020Review
- Allosteric modulators restore orthosteric agonist binding to mutated CBThe Journal of pharmacy and pharmacology · 2020Article
- Structure of an allosteric modulator bound to the CB1 cannabinoid receptor.Nature chemical biology · 2019Article
- Allosteric Modulation of Cannabinoid Receptor 1-Current Challenges and Future Opportunities.International journal of molecular sciences · 2019Review
- Identification of CB1 Receptor Allosteric Sites Using Force-Biased MMC Simulated Annealing and Validation by Structure-Activity Relationship Studies.ACS medicinal chemistry letters · 2019Article
- Discovery of Selective Cannabinoid CBSLAS discovery : advancing life sciences R & D · 2018Article
- The F238L Point Mutation in the Cannabinoid Type 1 Receptor Enhances Basal Endocytosis via Lipid Rafts.Frontiers in molecular neuroscience · 2018Article
- Article
- Chemogenomics knowledgebase and systems pharmacology for hallucinogen target identification-Salvinorin A as a case study.Journal of molecular graphics & modelling · 2016Article
- Article
- New paradigms in chemokine receptor signal transduction: Moving beyond the two-site model.Biochemical pharmacology · 2016Review
- Review
- Role of extracellular cysteine residues in the adenosine A2A receptor.Purinergic signalling · 2016Article
- Computational analysis of the CB1 carboxyl-terminus in the receptor-G protein complex.Proteins · 2016Article
- Computational Prediction and Biochemical Analyses of New Inverse Agonists for the CB1 Receptor.Journal of chemical information and modeling · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The seven transmembrane alpha-helices of G protein-coupled receptors (GPCRs) are the hallmark of this superfamily. Intrahelical interactions are critical to receptor assembly and, for the GPCR subclass that binds small molecules, ligand binding. Most research has focused on identifying the ligand binding pocket within the helical bundle, whereas the role of the extracellular loops remains undefined. Molecular modeling of the cannabinoid receptor 1 (CB1) extracellular loop 2 (EC2), however, suggests that EC2 is poised for key interactions. To test this possibility, we employed alanine scanning mutagenesis of CB1 EC2 and identified two distinct regions critical for ligand binding, G protein coupling activity, and receptor trafficking. Receptors with mutations in the N terminus of EC2 (W255A, N256A) were retained in the endoplasmic reticulum and did not bind the agonist (1R,3R,4R)-3-[2-hydroxy-4-(1,1-dimethylheptyl)-phenyl]-4-(3-hydroxypropyl)cyclohexan-1-ol (CP55940) or the inverse agonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide(SR141716A). In contrast, the C terminus of EC2 differentiates agonist and inverse agonist; the P269A, H270A, and I271A receptors exhibited diminished binding for several agonists but bound inverse agonists SR141716A, N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM251), and 4-[6-methoxy-2-(4-methoxyphenyl)benzofuran-3-carbonyl]benzonitrile (LY320135) with wild-type receptor affinity. The F268A receptor involving substitution in the Cys-X-X-X-Ar motif, displayed both impaired localization and ligand binding. Other amino acid substitutions at position 268 revealed that highly hydrophobic residues are required to accomplish both functions. It is noteworthy that a F268W receptor was trafficked to the cell surface yet displayed differential binding preference for inverse agonists comparable with the P269A, H270A, and I271A receptors. The findings are consistent with a dual role for EC2 in stabilizing receptor assembly and in ligand binding.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.