ArticlePloS one2013
G-protein coupled receptor 83 (GPR83) signaling determined by constitutive and zinc(II)-induced activity.
Article in PloS one, 2013. 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, 39 citations in OpenAlex.
- International Union of Basic and Clinical Pharmacology. CXXII. Applying an objective evaluation to the status of class A orphan G protein-coupled receptors.Pharmacological reviews · 2026Review
- Identification of small molecule ligands for GPR83 that modulate morphine antinociception and reward.Molecular pharmacology · 2026Article
- Exploring orphan GPCRs in neurodegenerative diseases.Frontiers in pharmacology · 2024Review
- Is the Neuropeptide PEN a Ligand of GPR83?International journal of molecular sciences · 2023Article
- Gpr83 Tunes Nociceptor Function, Controlling Pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Article
- Differential Roles of Extracellular Histidine Residues of GPR68 for Proton-Sensing and Allosteric Modulation by Divalent Metal Ions.Biochemistry · 2020Article
- Neuropeptide PEN and Its Receptor GPR83: Distribution, Signaling, and Regulation.ACS chemical neuroscience · 2019Review
- Evidence of G-protein-coupled receptor and substrate transporter heteromerization at a single molecule level.Cellular and molecular life sciences : CMLS · 2018Article
- Orphan neuropeptides and receptors: Novel therapeutic targets.Pharmacology & therapeutics · 2018Review
- Neuro-psychopharmacological perspective of Orphan receptors of Rhodopsin (class A) family of G protein-coupled receptors.Psychopharmacology · 2017Review
- Zinc Protects Oxidative Stress-Induced RPE Death by Reducing Mitochondrial Damage and Preventing Lysosome Rupture.Oxidative medicine and cellular longevity · 2017Article
- Identifying ligands at orphan GPCRs: current status using structure-based approaches.British journal of pharmacology · 2016Review
- Identification of GPR83 as the receptor for the neuroendocrine peptide PEN.Science signaling · 2016Article
- Zinc Is Involved in Depression by Modulating G Protein-Coupled Receptor Heterodimerization.Molecular neurobiology · 2016Article
- Insights into Basal Signaling Regulation, Oligomerization, and Structural Organization of the Human G-Protein Coupled Receptor 83.PloS one · 2016Article
- Ring Finger Protein 11 Inhibits Melanocortin 3 and 4 Receptor Signaling.Frontiers in endocrinology · 2016Article
- The extracellular N-terminal domain of G-protein coupled receptor 83 regulates signaling properties and is an intramolecular inverse agonist.BMC research notes · 2014Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The G-protein coupled receptor 83 (GPR83) is an orphan G-protein coupled receptor for which the natural ligand(s) and signaling pathway(s) remain to be identified. Previous studies suggest a role of GPR83 in the regulation of thermogenesis and the control of circulating adiponectin. The aim of this study was to gain insights into the molecular underpinnings underlying GPR83 signaling. In particular, we aimed to assess the underlying G-protein activated signaling pathway of GPR83 and how this pathway is affected by mutational activation and zinc(II) challenge. Finally, we assessed the capacity of GPR83 for homodimerization. Our results show for the first time that mouse (m) GPR83 has high basal Gq/11 activity without affecting Gi or Gs signaling. Furthermore, we found that, under physiological conditions, zinc(II) (but not calcium(II) and magnesium(II)) potently activates mGPR83, thus identifying zinc(II) as an endogenous molecule with agonistic capability to activate mGPR83. In line with the observation that zinc(II)-ions activate mGPR83, we identified a cluster of ion-binding sensitive amino acids (e.g. His145, His204, Cys207, Glu217) in an activation sensitive receptor region of mGPR83. The occurrence of a constitutive activating mutant and a zinc(II)-binding residue at the N-terminal part corroborate the importance of this region in mGPR83 signal regulation. Finally, our results indicate that mGPR83 forms homodimers, which extend the current knowledge and molecular facets of GPR83 signaling.
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