ArticleProceedings of the National Academy of Sciences of the United States of America2013
Critical role of parathyroid hormone (PTH) receptor-1 phosphorylation in regulating acute responses to PTH.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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58 citing papers in PubMed, 84 citations in OpenAlex.
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- G protein-coupled receptor signaling in osteogenic bone mesenchymal stem/stromal cells.Frontiers in cell and developmental biology · 2026Review
- Prolonging parathyroid hormone analog action in vitro and in vivo through peptide lipidation.Nature communications · 2025Article
- DimericeLife · 2025Article
- Eiken syndrome with parathyroid hormone resistance due to a novel parathyroid hormone receptor type 1 mutation: clinical features and functional analysis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Beneath the surface: endosomal GPCR signaling.Trends in biochemical sciences · 2024Review
- Highly biased agonism for GPCR ligands via nanobody tethering.Nature communications · 2024Article
- The Intricacies of Renal Phosphate Reabsorption-An Overview.International journal of molecular sciences · 2024Review
- Semi-synthetic nanobody-ligand conjugates exhibit tunable signaling properties and enhanced transcriptional outputs at neurokinin receptor-1.Protein science : a publication of the Protein Society · 2024Article
- Semi-synthetic nanobody-ligand conjugates exhibit tunable signaling properties and enhanced transcriptional outputs at neurokinin receptor-1.bioRxiv : the preprint server for biology · 2023Article
- Altered Signaling and Desensitization Responses in PTH1R Mutants Associated with Eiken Syndrome.Communications biology · 2023Article
- Molecular Mechanisms of PTH/PTHrP Class B GPCR Signaling and Pharmacological Implications.Endocrine reviews · 2023Article
- Molecular insights into the distinct signaling duration for the peptide-induced PTH1R activation.Nature communications · 2022Article
- Actions of Parathyroid Hormone Ligand Analogues in Humanized PTH1R Knockin Mice.Endocrinology · 2022Article
- Cell energy metabolism and bone formation.Bone reports · 2022Article
- Precise druggability of the PTH type 1 receptor.Nature chemical biology · 2022Article
- Activity-based, bioorthogonal imaging of phospholipase D reveals spatiotemporal dynamics of GPCR-Gq signaling.Cell chemical biology · 2022Article
- Cinacalcet may suppress kidney enlargement in hemodialysis patients with autosomal dominant polycystic kidney disease.Scientific reports · 2021Observational
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Agonist-induced phosphorylation of the parathyroid hormone (PTH) receptor 1 (PTHR1) regulates receptor signaling in vitro, but the role of this phosphorylation in vivo is uncertain. We investigated this role by injecting "knock-in" mice expressing a phosphorylation-deficient (PD) PTHR1 with PTH ligands and assessing acute biologic responses. Following injection with PTH (1-34), or with a unique, long-acting PTH analog, PD mice, compared with WT mice, exhibited enhanced increases in cAMP levels in the blood, as well as enhanced cAMP production and gene expression responses in bone and kidney tissue. Surprisingly, however, the hallmark hypercalcemic and hypophosphatemic responses were markedly absent in the PD mice, such that paradoxical hypocalcemic and hyperphosphatemic responses were observed, quite strikingly with the long-acting PTH analog. Spot urine analyses revealed a marked defect in the capacity of the PD mice to excrete phosphate, as well as cAMP, into the urine in response to PTH injection. This defect in renal excretion was associated with a severe, PTH-induced impairment in glomerular filtration, as assessed by the rate of FITC-inulin clearance from the blood, which, in turn, was explainable by an overly exuberant systemic hypotensive response. The overall findings demonstrate the importance in vivo of PTH-induced phosphorylation of the PTHR1 in regulating acute ligand responses, and they serve to focus attention on mechanisms that underlie the acute calcemic response to PTH and factors, such as blood phosphate levels, that influence it.
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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.