ArticleProceedings of the National Academy of Sciences of the United States of America2011
Wnt/β-catenin signaling is differentially regulated by Gα proteins and contributes to fibrous dysplasia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Molecular, phenotypic aspects and therapeutic horizons of rare genetic bone disorders.BioMed research international · 2014Pooled it
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- Injury-induced niche factors Cxcl12 and Shh/Ihh coordinate suture stem cell activation during calvarial bone regeneration.Science signaling · 2025Article
- G Protein-Coupled Receptor Signaling: Implications and Therapeutic Development Advances in Cancers.MedComm · 2025Review
- 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
- Fibrous dysplasia/McCune-Albright syndrome: state-of-the-art advances, pathogenesis, and basic/translational research.Orphanet journal of rare diseases · 2025Review
- Cross-union surgery for tibiofibular fractures in McCune-Albright syndrome: a case report and literature review.Frontiers in pediatrics · 2025Article
- Scoliosis as a Paradigm of Pathological Spinal Curvature: Molecular Mechanisms and Imaging Innovations : Molecular and Imaging Insights in Scoliosis.Galen medical journal · 2025Review
- Spatial Multi-omics Reveals the Role of the Wnt Modulator, Dkk2, in Palatogenesis'.Journal of dental research · 2024Article
- Wnt pathway inhibition with the porcupine inhibitor LGK974 decreases trabecular bone but not fibrosis in a murine model with fibrotic bone.JBMR plus · 2024Article
- Bio-integrated scaffold facilitates large bone regeneration dominated by endochondral ossification.Bioactive materials · 2024Article
- Increased Osteoblast GαJBMR plus · 2023Article
- A Rare Skeletal Disorder, Fibrous Dysplasia: A Review of Its Pathogenesis and Therapeutic Prospects.International journal of molecular sciences · 2023Review
- PTHrP Modulates the Proliferation and Osteogenic Differentiation of Craniofacial Fibrous Dysplasia-Derived BMSCs.International journal of molecular sciences · 2023Article
- Enhancer hijacking at the ARHGAP36 locus is associated with connective tissue to bone transformation.Nature communications · 2023Article
- LncRNA GNAS-AS1 knockdown inhibits keloid cells growth by mediating the miR-188-5p/RUNX2 axis.Molecular and cellular biochemistry · 2023Article
- Review
- Article
- Oncogene addiction to GNAS in GNASOncogene · 2022Article
- Nanostring technology on Fibrous Dysplasia bone biopsies. A pilot study suggesting different histology-related molecular profiles.Bone reports · 2022Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Skeletal dysplasias are common disabling disorders characterized by aberrant growth of bone and cartilage leading to abnormal skeletal structures and functions, often attributable to defects in skeletal progenitor cells. The underlying molecular and cellular mechanisms of most skeletal dysplasias remain elusive. Although the Wnt/β-catenin signaling pathway is required for skeletal progenitor cells to differentiate along the osteoblastic lineage, inappropriately elevated levels of signaling can also inhibit bone formation by suppressing osteoblast maturation. Here, we investigate interactions of the four major Gα protein families (Gα(s), Gα(i/o), Gα(q/11), and Gα(12/13)) with the Wnt/β-catenin signaling pathway and identify a causative role of Wnt/β-catenin signaling in fibrous dysplasia (FD) of bone, a disease that exhibits abnormal differentiation of skeletal progenitor cells. The activating Gα(s) mutations that cause FD potentiated Wnt/β-catenin signaling, and removal of Gα(s) led to reduced Wnt/β-catenin signaling and decreased bone formation. We further show that activation of Wnt/β-catenin signaling in osteoblast progenitors results in an FD-like phenotype and reduction of β-catenin levels rescued differentiation defects of FD patient-derived stromal cells. Gα proteins may act at the level of β-catenin destruction complex assembly by binding Axin. Our results indicate that activated Gα proteins differentially regulate Wnt/β-catenin signaling but, importantly, are not required core components of Wnt/β-catenin signaling. Our data suggest that activated Gα proteins are playing physiologically significant roles during both skeletal development and disease by modulating Wnt/β-catenin signaling strength.
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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.