ArticleThe Journal of biological chemistry2012
The cannabinoid receptor CB1 modulates the signaling properties of the lysophosphatidylinositol receptor GPR55.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- The Role of Cannabidiol in Liver Disease: A Systemic Review.International journal of molecular sciences · 2024Pooled it
- Integrative network analysis reveals organizational principles of the endocannabinoid system.Journal of cannabis research · 2026Article
- Astrocytic GPR55 receptors promote glycolysis.Journal of cannabis research · 2026Article
- Neuroprotective Role of Cannabinoid CBMolecular neurobiology · 2026Article
- Coactivation of CB1 and GPR55 promotes GABA release and motor behavior at striatonigral terminals through increased dimerization induced by CB1 activation.Frontiers in molecular neuroscience · 2026Article
- Cats and cannabinoids: past, present and future.Journal of feline medicine and surgery · 2025Review
- In Vitro Signaling Properties of Cannabinoid and Orexin Receptors: How Orexin Receptors Influence Cannabinoid Receptor-Mediated Signaling.Pharmacology research & perspectives · 2025Article
- Expression, Distribution and Function of the Transient Receptor Potential Vanilloid Type 1 (TRPV1) in Endometrial Cancer.International journal of molecular sciences · 2025Article
- From Classical to Alternative Pathways of 2-Arachidonoylglycerol Synthesis: AlterAGs at the Crossroad of Endocannabinoid and Lysophospholipid Signaling.Molecules (Basel, Switzerland) · 2024Review
- Cannabinoids: Potential for Modulation and Enhancement When Combined with Vitamin B12 in Case of Neurodegenerative Disorders.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The Interaction of the Endocannabinoid Anandamide and Paracannabinoid Lysophosphatidylinositol during Cell Death Induction in Human Breast Cancer Cells.International journal of molecular sciences · 2024Article
- Article
- Cannabidiol modulates excitatory-inhibitory ratio to counter hippocampal hyperactivity.Neuron · 2023Article
- The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells.International journal of molecular sciences · 2023Article
- Lysophosphatidylinositol Induced Morphological Changes and Stress Fiber Formation through the GPR55-RhoA-ROCK Pathway.International journal of molecular sciences · 2022Article
- Novel Noninvasive Approaches to the Treatment of Obesity: From Pharmacotherapy to Gene Therapy.Endocrine reviews · 2022Review
- Non-Canonical Cannabinoid Receptors with Distinct Binding and Signaling Properties in Prostate and Other Cancer Cell Types Mediate Cell Death.International journal of molecular sciences · 2022Article
- Targeting the Endocannabinoidome in Pancreatic Cancer.Biomolecules · 2022Review
- Pan-phylumFrontiers in endocrinology · 2022Article
- The anticonvulsant phytocannabinoids CBGVA and CBDVA inhibit recombinant T-type channels.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
The G protein-coupled receptor (GPCR) 55 (GPR55) and the cannabinoid receptor 1 (CB1R) are co-expressed in many tissues, predominantly in the central nervous system. Seven transmembrane spanning (7TM) receptors/GPCRs can form homo- and heteromers and initiate distinct signaling pathways. Recently, several synthetic CB1 receptor inverse agonists/antagonists, such as SR141716A, AM251, and AM281, were reported to activate GPR55. Of these, SR141716A was marketed as a promising anti-obesity drug, but was withdrawn from the market because of severe side effects. Here, we tested whether GPR55 and CB1 receptors are capable of (i) forming heteromers and (ii) whether such heteromers could exhibit novel signaling patterns. We show that GPR55 and CB1 receptors alter each others signaling properties in human embryonic kidney (HEK293) cells. We demonstrate that the co-expression of FLAG-CB1 receptors in cells stably expressing HA-GPR55 specifically inhibits GPR55-mediated transcription factor activation, such as nuclear factor of activated T-cells and serum response element, as well as extracellular signal-regulated kinases (ERK1/2) activation. GPR55 and CB1 receptors can form heteromers, but the internalization of both receptors is not affected. In addition, we observe that the presence of GPR55 enhances CB1R-mediated ERK1/2 and nuclear factor of activated T-cell activation. Our data provide the first evidence that GPR55 can form heteromers with another 7TM/GPCR and that this interaction with the CB1 receptor has functional consequences in vitro. The GPR55-CB1R heteromer may play an important physiological and/or pathophysiological role in tissues endogenously co-expressing both receptors.
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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.