ArticleThe Journal of biological chemistry2011
Runx2 protein expression utilizes the Runx2 P1 promoter to establish osteoprogenitor cell number for normal bone formation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 66 citations in OpenAlex.
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- Hyperoside Modulates the Estrogen-PI3K/VEGF Axis to Ameliorate Oxidative Damage-Induced Inhibition of Bone Formation in MC3T3-E1 Cells.Immunity, inflammation and disease · 2026Article
- Time-Course Evaluation of the In Vivo Resorption Process of Calcium Phosphates/Poly(lactide-International journal of molecular sciences · 2026Article
- Size-Dependent Layered Double Hydroxide Nanoparticles Promote Osteogenesis and Bone Regeneration via METTL3-Dependent N6-Methyladenosine Modification of Runx2 mRNA.International journal of nanomedicine · 2026Article
- Branch site mutated mice revealed distinct roles of two Runx2 isoforms in bone development.Frontiers in cell and developmental biology · 2026Article
- Management strategies for fluoride toxicity and the critical role of epigenetic therapy.Molecular biology reports · 2025Review
- Trabecular Titanium Architecture Drives Human Mesenchymal Stem Cell Proliferation and Bone Differentiation.International journal of molecular sciences · 2025Article
- An Osteoblast-Specific Enhancer and Subenhancer Cooperatively RegulateInternational journal of molecular sciences · 2025Article
- Non-Canonical TERT Activity Initiates Osteogenesis in Calcific Aortic Valve Disease.Circulation research · 2025Article
- CCAAT/Enhancer-Binding Protein β (C/EBPβ) Regulates Calcium Deposition in Smooth Muscle Cells.International journal of molecular sciences · 2024Article
- MicroRNAs in fluorosis pathogenesis: impact on dental, skeletal, and soft tissues.Archives of toxicology · 2024Review
- New Genetic Variants ofBiology · 2024Article
- Mechanism of MiR-145a-3p/Runx2 pathway in dexamethasone impairment of MC3T3-E1 osteogenic capacity in mice.PloS one · 2024Article
- 3D-Printed β-Tricalcium Phosphate Scaffolds Promote Osteogenic Differentiation of Bone Marrow-Deprived Mesenchymal Stem Cells in an N6-methyladenosine-Dependent Manner.International journal of bioprinting · 2022Article
- Genetic Pattern, Orthodontic and Surgical Management of Multiple Supplementary Impacted Teeth in a Rare, Cleidocranial Dysplasia Patient: A Case Report.Medicina (Kaunas, Lithuania) · 2021Article
- Transcriptional Programming in Arteriosclerotic Disease: A Multifaceted Function of the Runx2 (Runt-Related Transcription Factor 2).Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Article
- Elevated BMP and Mechanical Signaling Through YAP1/RhoA Poises FOP Mesenchymal Progenitors for Osteogenesis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- ERα and Wnt/β‑catenin signaling pathways are involved in angelicin‑dependent promotion of osteogenesis.Molecular medicine reports · 2019Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
The Runt-related transcription factor, Runx2, is essential for osteogenesis and is controlled by both distal (P1) and proximal (P2) promoters. To understand Runx2 function requires determination of the spatiotemporal activity of P1 and P2 to Runx2 protein production. We generated a mouse model in which the P1-derived transcript was replaced with a lacZ reporter allele, resulting in loss of P1-derived protein while simultaneously allowing discrimination between the activities of the two promoters. Loss of P1-driven expression causes developmental defects with cleidocranial dysplasia-like syndromes that persist in the postnatal skeleton. P1 activity is robust in preosteogenic mesenchyme and at the onset of bone formation but decreases as bone matures. Homozygous Runx2-P1(lacZ/lacZ) mice have a normal life span but exhibit severe osteopenia and compromised bone repair in adult mice because of osteoblastic defects and not increased osteoclastic resorption. Gene expression profiles of bone, immunohistochemical studies, and ex vivo differentiation using calvarial osteoblasts and marrow stromal cells identified mechanisms for the skeletal phenotype. The findings indicate that P1 promoter activity is necessary for generating a threshold level of Runx2 protein to commit sufficient osteoprogenitor numbers for normal bone formation. P1 promoter function is not compensated via the P2 promoter. However, the P2 transcript with compensatory mechanisms from bone morphogenetic protein (BMP) and Wnt signaling is adequate for mineralization of the bone tissue that does form. We conclude that selective utilization of the P1 and P2 promoters enables the precise spatiotemporal expression of Runx2 necessary for normal skeletogenesis and the maintenance of bone mass in the adult.
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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.