ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2017
Orphan Adhesion GPCR GPR64/ADGRG2 Is Overexpressed in Parathyroid Tumors and Attenuates Calcium-Sensing Receptor-Mediated Signaling.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- A Novel piRNA-Mediated Epigenetic Axis: piR-36241 Exacerbates Pulpitis by Silencing the Protective Receptor ADGRG2 in Human Dental Pulp Stem Cells.International endodontic journal · 2026Article
- Exploring the Binding Mechanism of ADGRG2 Through Metadynamics and Biochemical Analysis.International journal of molecular sciences · 2024Article
- Article
- KMT2A and chronic inflammation as potential drivers of sporadic parathyroid adenoma.Clinical and translational medicine · 2024Article
- Mechanistic Insights into Peptide Binding and Deactivation of an Adhesion G Protein-Coupled Receptor.Molecules (Basel, Switzerland) · 2023Article
- Molecular Genetic Aspects of Sporadic Multiglandular Primary Hyperparathyroidism.Physiological research · 2023Review
- Adhesion G Protein-Coupled Receptor G2 Promotes Hepatocellular Carcinoma Progression and Serves as a Neutrophil-Related Prognostic Biomarker.International journal of molecular sciences · 2023Article
- Proteomic approach towards identification of seminal fluid biomarkers from individuals with severe oligozoospermia, cryptozoospermia and non-obstructive azoospermia: a pilot study.Translational andrology and urology · 2023Article
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- Identification of small extracellular vesicle protein biomarkers for pediatric Ewing Sarcoma.Frontiers in molecular biosciences · 2023Article
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- Immunohistochemical Profile of Parathyroid Tumours: A Comprehensive Review.International journal of molecular sciences · 2022Review
- Molecular Mechanisms of Parathyroid Disorders in Chronic Kidney Disease.Metabolites · 2022Review
- Evaluating the feasibility of Cas9 overexpression in 3T3-L1 cells for generation of genetic knock-out adipocyte cell lines.Adipocyte · 2021Article
- Conserved residues in the extracellular loop 2 regulate Stachel-mediated activation of ADGRG2.Scientific reports · 2021Article
- Heterogeneity of G protein activation by the calcium-sensing receptor.Journal of molecular endocrinology · 2021Article
- Genetics of the congenital absence of the vas deferens.Human genetics · 2021Review
- Function and therapeutic potential of G protein-coupled receptors in epididymis.British journal of pharmacology · 2020Review
- The repertoire of Adhesion G protein-coupled receptors in adipocytes and their functional relevance.International journal of obesity (2005) · 2020Article
- Adhesion GPCRs as a paradigm for understanding polycystin-1 G protein regulation.Cellular signalling · 2020Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Abnormal feedback of serum calcium to parathyroid hormone (PTH) secretion is the hallmark of primary hyperparathyroidism (PHPT). Although the molecular pathogenesis of parathyroid neoplasia in PHPT has been linked to abnormal expression of genes involved in cell growth (e.g., cyclin D1, retinoblastoma, and β-catenin), the molecular basis of abnormal calcium sensing by calcium-sensing receptor (CaSR) and PTH hypersecretion in PHPT are incompletely understood. Through gene expression profiling, we discovered that an orphan adhesion G protein-coupled receptor (GPCR), GPR64/ADGRG2, is expressed in human normal parathyroid glands and is overexpressed in parathyroid tumors from patients with PHPT. Using immunohistochemistry, Western blotting, and coimmunoprecipitation, we found that GPR64 is expressed on the cell surface of parathyroid cells, is overexpressed in parathyroid tumors, and physically interacts with the CaSR. By using reporter gene assay and GPCR second messenger readouts we identified Gαs, 3',5'-cyclic adenosine monophosphate (cAMP), protein kinase A, and cAMP response element binding protein (CREB) as the signaling cascade downstream of GPR64. Furthermore, we found that an N-terminally truncated human GPR64 is constitutively active and a 15-amino acid-long peptide C-terminal to the GPCR proteolysis site (GPS) of GPR64 activates this receptor. Functional characterization of GPR64 demonstrated its ability to increase PTH release from human parathyroid cells at a range of calcium concentrations. We discovered that the truncated constitutively active, but not the full-length GPR64 physically interacts with CaSR and attenuates the CaSR-mediated intracellular Ca
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