Abstract
Bone-specific transcription of the osteocalcin (OC) gene is principally regulated by the Runx2 transcription factor and further stimulated in response to 1α,25-dihydroxy Vitamin D3 via its specific receptor (VDR). The rat OC gene promoter contains three recognition sites for Runx2 (sites A-C). Mutation of sites A and B, which flank the 1α,25-dihydroxy Vitamin D3-responsive element (VDRE), abolishes 1α,25-dihydroxy Vitamin D3-dependent enhancement of OC transcription, indicating a tight functional relationship between VDR and Runx2 factors. Additionally, the transcriptional co-activator p300 is recruited to the OC promoter by Runx2 where it up-regulates both basal and 1α,25-dihydroxy Vitamin D3-enhanced OC expression. Here, we present an overview of how in osteoblastic cells expressing OC, Runx2 modulates the 1α,25-dihydroxy Vitamin D3-dependent stimulation of the OC promoter by first recruiting transcriptional co-activators and then by further stabilizing the interaction of the VDR with the VDRE.
Original language | English |
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Pages (from-to) | 269-271 |
Number of pages | 3 |
Journal | Journal of Steroid Biochemistry and Molecular Biology |
Volume | 89-90 |
DOIs | |
Publication status | Published - May 2004 |
Keywords
- Osteocalcin
- Runx2
- Transcription
- Vitamin D
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Biochemistry
- Molecular Medicine
- Molecular Biology
- Endocrinology
- Clinical Biochemistry
- Cell Biology