ArticleMolecular endocrinology (Baltimore, Md.)2011
Regulator of G protein signaling 5 is highly expressed in parathyroid tumors and inhibits signaling by the calcium-sensing receptor.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Measuring Calcium-Sensing Receptor Agonist-Driven Insertional Signaling (ADIS) and Trafficking by TIRF Microscopy.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Function and regulation of RGS family members in solid tumours: a comprehensive review.Cell communication and signaling : CCS · 2023Review
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor.BMC surgery · 2023Article
- Implications of regulator of G-protein signaling 5 expression in the pathogenesis of primary and secondary hyperparathyroidism.BMC endocrine disorders · 2022Article
- Effect of Regulator of G Protein Signaling Proteins on Bone.Frontiers in endocrinology · 2022Review
- Ex Vivo Intact Tissue Analysis Reveals Alternative Calcium-sensing Behaviors in Parathyroid Adenomas.The Journal of clinical endocrinology and metabolism · 2021Article
- Autoantibodies Against the Purkinje Cell Protein RGS8 in Paraneoplastic Cerebellar Syndrome.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- Intratumor heterogeneity in human parathyroid tumors.Histology and histopathology · 2020Review
- International Union of Basic and Clinical Pharmacology. CVIII. Calcium-Sensing Receptor Nomenclature, Pharmacology, and Function.Pharmacological reviews · 2020Review
- RGS5 plays a significant role in renal cell carcinoma.Royal Society open science · 2020Article
- Parathyroid-Targeted Overexpression of Regulator of G-Protein Signaling 5 (RGS5) Causes Hyperparathyroidism in Transgenic Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Calcium-sensing receptor in colorectal inflammation and cancer: Current insights and future perspectives.World journal of gastroenterology · 2018Review
- Transcriptional profiling reveals distinct classes of parathyroid tumors in PHPT.Endocrine-related cancer · 2018Article
- Orphan Adhesion GPCR GPR64/ADGRG2 Is Overexpressed in Parathyroid Tumors and Attenuates Calcium-Sensing Receptor-Mediated Signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- PTH and Vitamin D.Comprehensive Physiology · 2016Review
- Single-cell functional analysis of parathyroid adenomas reveals distinct classes of calcium sensing behaviour in primary hyperparathyroidism.Journal of cellular and molecular medicine · 2016Article
- A Novel Ex Vivo Method for Visualizing Live-Cell Calcium Response Behavior in Intact Human Tumors.PloS one · 2016Article
- The pericyte antigen RGS5 in perivascular soft tissue tumors.Human pathology · 2016Article
- Role of Regulators of G Protein Signaling Proteins in Bone Physiology and Pathophysiology.Progress in molecular biology and translational science · 2015Review
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
Abstract
The molecular mechanisms responsible for aberrant calcium signaling in parathyroid disease are poorly understood. The loss of appropriate calcium-responsive modulation of PTH secretion observed in parathyroid disease is commonly attributed to decreased expression of the calcium-sensing receptor (CaSR), a G protein-coupled receptor. However, CaSR expression is highly variable in parathyroid adenomas, and the lack of correlation between CaSR abundance and calcium-responsive PTH kinetics indicates that mechanisms independent of CaSR expression may contribute to aberrant calcium sensing in parathyroid disease. To gain a better understanding of parathyroid tumors and the molecular determinants that drive parathyroid adenoma development, we performed gene expression profiling on a panel of 64 normal and neoplastic parathyroid tissues. The microarray data revealed high-level expression of genes known to be involved in parathyroid biology (PTH, VDR, CGA, CaSR, and GCM2). Moreover, our screen identified regulator of G protein signaling 5 (RGS5) as a candidate inhibitor of CaSR signaling. We confirmed RGS5 to be highly expressed in parathyroid adenomas relative to matched-pair normal glands. Transient expression of RGS5 in cells stably expressing CaSR resulted in dose-dependent abrogation of calcium-stimulated inositol trisphosphate production and ERK1/2 phosphorylation. Furthermore, we found that RGS5-nullizygous mice display reduced plasma PTH levels, an outcome consistent with attenuated opposition to CaSR activity. Collectively, these data suggest that RGS5 can act as a physiological regulator of calcium sensing by CaSR in the parathyroid gland. The abnormally elevated expression of RGS5 observed in parathyroid adenomas could thus represent a novel mechanism of CaSR desensitization in patients with primary hyperparathyroidism.
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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.