ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2010
Gs G protein-coupled receptor signaling in osteoblasts elicits age-dependent effects on bone formation.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
26 citing papers in PubMed, 30 citations in OpenAlex.
- G protein-coupled receptor signaling in osteogenic bone mesenchymal stem/stromal cells.Frontiers in cell and developmental biology · 2026Review
- Single-cell analysis of human fibrous dysplasia bone reveals a fibrotic transcriptome and GNAS variants in endothelial, perivascular, and stromal cells.American journal of human genetics · 2025Article
- Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia.Nature communications · 2025Article
- Wnt pathway inhibition with the porcupine inhibitor LGK974 decreases trabecular bone but not fibrosis in a murine model with fibrotic bone.JBMR plus · 2024Article
- Revolutionizing bone regeneration: advanced biomaterials for healing compromised bone defects.Frontiers in aging · 2023Review
- Inactivation of Osteoblast PKC Signaling Reduces Cortical Bone Mass and Density and Aggravates Renal Osteodystrophy in Mice with Chronic Kidney Disease on High Phosphate Diet.International journal of molecular sciences · 2022Article
- GPR125 positively regulates osteoclastogenesis potentially through AKT-NF-κB and MAPK signaling pathways.International journal of biological sciences · 2022Article
- Fibrous Dysplasia/McCune-Albright Syndrome: A Rare, Mosaic Disease of Gα s Activation.Endocrine reviews · 2020Review
- Fibrous Dysplasia of Bone and McCune-Albright Syndrome: A Bench to Bedside Review.Calcified tissue international · 2019Review
- Advances in Models of Fibrous Dysplasia/McCune-Albright Syndrome.Frontiers in endocrinology · 2019Review
- Fibrous dysplasia of bone: craniofacial and dental implications.Oral diseases · 2017Review
- Heterotrimeric G proteins in the control of parathyroid hormone actions.Journal of molecular endocrinology · 2017Review
- Article
- Gs/Gi Regulation of Bone Cell Differentiation: Review and Insights from Engineered Receptors.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2016Review
- Fibrous Dysplasia/McCune-Albright Syndrome: Clinical and Translational Perspectives.Current osteoporosis reports · 2016Review
- Increased Gs Signaling in Osteoblasts Reduces Bone Marrow and Whole-Body Adiposity in Male Mice.Endocrinology · 2016Article
- Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy.The Journal of biological chemistry · 2016Article
- Assessing the osteoblast transcriptome in a model of enhanced bone formation due to constitutive Gs-G protein signaling in osteoblasts.Experimental cell research · 2015Article
- Constitutive expression of Gsα(R201C) in mice produces a heritable, direct replica of human fibrous dysplasia bone pathology and demonstrates its natural history.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014Article
- Disrupted bone remodeling leads to cochlear overgrowth and hearing loss in a mouse model of fibrous dysplasia.PloS one · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Age-dependent changes in skeletal growth are important for regulating skeletal expansion and determining peak bone mass. However, how G protein-coupled receptors (GPCRs) regulate these changes is poorly understood. Previously, we described a mouse model expressing Rs1, an engineered receptor with high basal G(s) activity. Rs1 expression in osteoblasts induced a dramatic age-dependent increase in trabecular bone with features resembling fibrous dysplasia. To further investigate how activation of the G(s)-GPCR pathway affects bone formation at different ages, we used the tetracycline-inducible system in the ColI(2.3)(+)/Rs1(+) mouse model to control the timing of Rs1 expression. We found that the Rs1 phenotype developed rapidly between postnatal days 4 and 6, that delayed Rs1 expression resulted in attenuation of the Rs1 phenotype, and that the Rs1-induced bone growth and deformities were markedly reversed when Rs1 expression was suppressed in adult mice. These findings suggest a distinct window of increased osteoblast responsiveness to G(s) signaling during the early postnatal period. In addition, adult bones encode information about their normal shape and structure independently from mechanisms regulating bone expansion. Finally, our model provides a powerful tool for investigating the effects of continuous G(s)-GPCR signaling on dynamic bone growth and remodeling.
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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.