ArticleMolecular and cellular biology2004
Bone-specific transcription factor Runx2 interacts with the 1alpha,25-dihydroxyvitamin D3 receptor to up-regulate rat osteocalcin gene expression in osteoblastic cells.
Article in Molecular and cellular biology, 2004. 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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Who cites it
62 citing papers in PubMed, 132 citations in OpenAlex.
- The role and therapeutic potential of vitamins in fracture healing.Nutrition journal · 2026Review
- Genome-wide analysis reveals ligand-dependent allostery in RARα:RXR-mediated transcriptional regulation.Cell reports · 2026Article
- Atoh8 expression inhibition promoted osteogenic differentiation of ADSCs and inhibited cell proliferation in vitro and rat bone defect models.Adipocyte · 2025Article
- Osteocalcin and GPR158: linking bone and brain function.Frontiers in cell and developmental biology · 2025Review
- MicroRNAs in fluorosis pathogenesis: impact on dental, skeletal, and soft tissues.Archives of toxicology · 2024Review
- Investigating the potential effect of Holothuria scabra extract on osteogenic differentiation in preosteoblast MC3T3-E1 cells.Scientific reports · 2024Article
- "A Friend Among Strangers" or the Ambiguous Roles of Runx2.Biomolecules · 2024Review
- Roles of osteocalcin in the central nervous system.CNS neuroscience & therapeutics · 2024Review
- Daytime administration of melatonin has better protective effects on bone loss in ovariectomized rats.Journal of orthopaedic surgery and research · 2023Article
- Targeting Sirt1, AMPK, Nrf2, CK2, and Soluble Guanylate Cyclase with Nutraceuticals: A Practical Strategy for Preserving Bone Mass.International journal of molecular sciences · 2022Review
- Epigenetic-Mediated Regulation of Gene Expression for Biological Control and Cancer: Cell and Tissue Structure, Function, and Phenotype.Results and problems in cell differentiation · 2022Review
- Bone mineral density, bone microstructure, and bone turnover markers in females with temporomandibular joint osteoarthritis.Clinical oral investigations · 2021Article
- Effects of Extracellular Osteoanabolic Agents on the Endogenous Response of Osteoblastic Cells.Cells · 2021Review
- Bio-Functionalized Chitosan for Bone Tissue Engineering.International journal of molecular sciences · 2021Article
- Genetic response to low‑intensity ultrasound on mouse ST2 bone marrow stromal cells.Molecular medicine reports · 2021Article
- Switches in histone modifications epigenetically control vitamin D3-dependent transcriptional upregulation of the CYP24A1 gene in osteoblastic cells.Journal of cellular physiology · 2020Article
- Ezh2-dependent H3K27me3 modification dynamically regulates vitamin D3-dependent epigenetic control of CYP24A1 gene expression in osteoblastic cells.Journal of cellular physiology · 2020Article
- Dual usage of a stage-specific fluorescent reporter system based on a helper-dependent adenoviral vector to visualize osteogenic differentiation.Scientific reports · 2019Article
- 1,25(OH)FASEB bioAdvances · 2019Article
- Mll-COMPASS complexes mediate H3K4me3 enrichment and transcription of the osteoblast master gene Runx2/p57 in osteoblasts.Journal of cellular physiology · 2019Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Bone-specific transcription of the osteocalcin (OC) gene is regulated principally by the Runx2 transcription factor and is further stimulated in response to 1alpha,25-dihydroxyvitamin D3 via its specific receptor (VDR). The rat OC gene promoter contains three recognition sites for Runx2 (sites A, B, and C). Mutation of sites A and B, which flank the 1alpha,25-dihydroxyvitamin D3-responsive element (VDRE), abolishes 1alpha,25-dihydroxyvitamin D3-dependent enhancement of OC transcription, indicating a tight functional relationship between the VDR and Runx2 factors. In contrast to most of the members of the nuclear receptor family, VDR possesses a very short N-terminal A/B domain, which has led to the suggestion that its N-terminal region does not contribute to transcriptional enhancement. Here, we have combined transient-overexpression, coimmunoprecipitation, in situ colocalization, chromatin immunoprecipitation, and glutathione S-transferase pull-down analyses to demonstrate that in osteoblastic cells expressing OC, VDR interacts directly with Runx2 bound to site B, which is located immediately adjacent to the VDRE. This interaction contributes significantly to 1alpha,25-dihydroxyvitamin D3-dependent enhancement of the OC promoter and requires a region located C terminal to the runt homology DNA binding domain of Runx2 and the N-terminal region of VDR. Together, our results indicate that Runx2 plays a key role in the 1alpha,25-dihydroxyvitamin D3-dependent stimulation of the OC promoter in osteoblastic cells by further stabilizing the interaction of the VDR with the VDRE. These studies demonstrate a novel mechanism for combinatorial control of bone tissue-specific gene expression. This mechanism involves the intersection of two major pathways: Runx2, a "master" transcriptional regulator of osteoblast differentiation, and 1alpha,25-dihydroxyvitamin D3, a hormone that promotes expression of genes associated with these terminally differentiated bone cells.
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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.