ArticleThe Journal of cell biology2011
Control of bone formation by the serpentine receptor Frizzled-9.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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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.
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Who cites it
62 citing papers in PubMed, 112 citations in OpenAlex.
- Identification of candidate receptors mediating the osteoanabolic influence of Wnt1.JBMR plus · 2026Article
- Inhibition of AXL receptor tyrosine kinase increases osteoblast function and bone mass.Bone research · 2026Article
- Extracellular matrix dysregulation in aging, calcification, and cancer diseases: insights into cellular senescence, inflammation, and novel therapeutic strategies.International journal of biological sciences · 2025Review
- Osteomodulin deficiency in mice causes a specific reduction of transversal cortical bone size.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and disease.Bone research · 2024Review
- Design principles and therapeutic applications of novel synthetic WNT signaling agonists.iScience · 2024Review
- Endothelial to mesenchymal Notch signaling regulates skeletal repair.JCI insight · 2024Article
- Klf10 is involved in extracellular matrix calcification of chondrocytes alleviating chondrocyte senescence.Journal of translational medicine · 2024Article
- Emerging Landscape of Osteogenesis Imperfecta Pathogenesis and Therapeutic Approaches.ACS pharmacology & translational science · 2024Review
- Cholesteatoma Severely Impacts the Integrity and Bone Material Quality of the Incus.Calcified tissue international · 2023Article
- Mesoporous Bioactive Glass-Incorporated Injectable Strontium-Containing Calcium Phosphate Cement Enhanced Osteoconductivity in a Critical-Sized Metaphyseal Defect in Osteoporotic Rats.Bioengineering (Basel, Switzerland) · 2023Article
- AXIN1 bi-allelic variants disrupting the C-terminal DIX domain cause craniometadiaphyseal osteosclerosis with hip dysplasia.American journal of human genetics · 2023Article
- Wnt signaling: Essential roles in osteoblast differentiation, bone metabolism and therapeutic implications for bone and skeletal disorders.Genes & diseases · 2023Review
- CUL4B orchestrates mesenchymal stem cell commitment by epigenetically repressing KLF4 and C/EBPδ.Bone research · 2023Article
- WNT11, a new gene associated with early onset osteoporosis, is required for osteoblastogenesis.Human molecular genetics · 2022Article
- The Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase Pathway in Osteoblasts.Journal of bone metabolism · 2022Article
- Frizzled receptors in melanomagenesis: From molecular interactions to target identification.Frontiers in oncology · 2022Review
- Prevention of Hypomineralization In Auditory Ossicles of Vitamin D Receptor (Vdr) Deficient Mice.Frontiers in endocrinology · 2022Article
- Loss of Frizzled 9 in Lung Cells Alters Epithelial Phenotype and Promotes Premalignant Lesion Development.Frontiers in oncology · 2022Article
- The WNT1Bone research · 2021Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although Wnt signaling in osteoblasts is of critical importance for the regulation of bone remodeling, it is not yet known which specific Wnt receptors of the Frizzled family are functionally relevant in this process. In this paper, we show that Fzd9 is induced upon osteoblast differentiation and that Fzd9(-/-) mice display low bone mass caused by impaired bone formation. Our analysis of Fzd9(-/-) primary osteoblasts demonstrated defects in matrix mineralization in spite of normal expression of established differentiation markers. In contrast, we observed a reduced expression of chemokines and interferon-regulated genes in Fzd9(-/-) osteoblasts. We also identified the ubiquitin-like modifier Isg15 as one potential downstream mediator of Fzd9 in these cells. Importantly, our molecular analysis further revealed that canonical Wnt signaling is not impaired in the absence of Fzd9, thus explaining the absence of a bone resorption phenotype. Collectively, our results reveal a previously unknown function of Fzd9 in osteoblasts, a finding that may have therapeutic implications for bone loss disorders.
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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.