ArticleJournal of cellular biochemistry2011
The mouse RANKL gene locus is defined by a broad pattern of histone H4 acetylation and regulated through distinct distal enhancers.
Article in Journal of cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Consensus Statement on Vitamin D Status Assessment and Supplementation: Whys, Whens, and Hows.Endocrine reviews · 2024Article
- Genomic mechanisms controlling renal vitamin D metabolism.The Journal of steroid biochemistry and molecular biology · 2023Article
- Vitamin D: Newer Concepts of Its Metabolism and Function at the Basic and Clinical Level.Journal of the Endocrine Society · 2020Article
- Sex-determining region Y (SRY) attributes to gender differences in RANKL expression and incidence of osteoporosis.Experimental & molecular medicine · 2019Article
- Parathyroid hormone(1-34) and its analogs differentially modulate osteoblasticThe Journal of biological chemistry · 2018Article
- A Novel Distal Enhancer Mediates Inflammation-, PTH-, and Early Onset Murine Kidney Disease-Induced Expression of the MouseJBMR plus · 2018Article
- Biology and Mechanisms of Action of the Vitamin D Hormone.Endocrinology and metabolism clinics of North America · 2017Review
- SIKs control osteocyte responses to parathyroid hormone.Nature communications · 2016Article
- Deletion of the Distal Tnfsf11 RL-D2 Enhancer That Contributes to PTH-Mediated RANKL Expression in Osteoblast Lineage Cells Results in a High Bone Mass Phenotype in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016Article
- Unique Distal Enhancers Linked to the Mouse Tnfsf11 Gene Direct Tissue-Specific and Inflammation-Induced Expression of RANKL.Endocrinology · 2016Article
- A DNA segment spanning the mouse Tnfsf11 transcription unit and its upstream regulatory domain rescues the pleiotropic biologic phenotype of the RANKL null mouse.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
- Pleiotropic Activities of Vitamin D Receptors - Adequate Activation for Multiple Health Outcomes.The Clinical biochemist. Reviews · 2015Review
- Vitamin D and alternative splicing of RNA.The Journal of steroid biochemistry and molecular biology · 2015Review
- Fundamentals of vitamin D hormone-regulated gene expression.The Journal of steroid biochemistry and molecular biology · 2014Review
- The osteoblast to osteocyte transition: epigenetic changes and response to the vitamin D3 hormone.Molecular endocrinology (Baltimore, Md.) · 2014Article
- The RUNX2 cistrome in osteoblasts: characterization, down-regulation following differentiation, and relationship to gene expression.The Journal of biological chemistry · 2014Article
- Coregulation of genetic programs by the transcription factors NFIB and STAT5.Molecular endocrinology (Baltimore, Md.) · 2014Article
- Regulation of gene expression by 1,25-dihydroxyvitamin D3 in bone cells: exploiting new approaches and defining new mechanisms.BoneKEy reports · 2014Review
- Progesterone receptor and Stat5 signaling cross talk through RANKL in mammary epithelial cells.Molecular endocrinology (Baltimore, Md.) · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
RANKL is a stromal cell-derived tumor necrosis factor (TNF)-like factor that plays a primary role in osteoclast formation and function. Recent studies suggest that 1,25(OH)(2) D(3) induces Rankl expression via vitamin D receptor (VDR) interaction at several enhancers located up to 76 kb upstream of the gene's transcriptional start site (TSS). In the current studies, we explored these interactions further using ChIP-chip and RNA analysis. We confirm VDR and RXR binding to the five enhancers described previously and identify two additional sites, one located within the Rankl coding region. We also show that RNA polymerase II is recruited to these enhancers, most likely through transcription factors TBP, TFIIB, and TAF(II) 250. Interestingly, the recruitment of these factors leads to the production of RNA transcripts, although their role at present is unknown. We also discovered that histone H4 acetylation (H4ac) marks many upstream Rankl enhancers under basal conditions and that H4ac is increased upon 1,25(OH)(2) D(3) treatment. Surprisingly, the hormone also induces C/EBPβ binding across the Rankl locus. C/EBPβ binding correlates directly with increased H4ac activity following 1,25(OH)(2) D(3) treatment. Finally, elevated H4ac is restricted to an extended region located between two potential insulator sites occupied by CTCF and Rad21. These data suggest a mechanism whereby 1,25(OH)(2) D(3) functions via the VDR and C/EBPβ to upregulate Rankl expression.
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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.