ArticleProceedings of the National Academy of Sciences of the United States of America2005
Regulation of relB in dendritic cells by means of modulated association of vitamin D receptor and histone deacetylase 3 with the promoter.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 93 citations in OpenAlex.
- The Effects of Vitamin D Supplementation on Metabolic and Oxidative Stress Markers in Patients With Type 2 Diabetes: A 6-Month Follow Up Randomized Controlled Study.Frontiers in endocrinology · 2021Trial
- Nuclear receptors as novel regulators that modulate cancer radiosensitivity and normal tissue radiotoxicity.Molecular cancer · 2025Review
- Review
- Non-canonical NF-κB signaling limits the tolerogenic β-catenin-Raldh2 axis in gut dendritic cells to exacerbate intestinal pathologies.The EMBO journal · 2024Article
- A Review: Highlighting the Links between Epigenetics, COVID-19 Infection, and Vitamin D.International journal of molecular sciences · 2022Review
- Consideration of possible effects of vitamin D on established cancer, with reference to malignant melanoma.Pigment cell & melanoma research · 2022Review
- The Role of Histone Deacetylase 3 Complex in Nuclear Hormone Receptor Action.International journal of molecular sciences · 2021Review
- Preclinical and clinical progress for HDAC as a putative target for epigenetic remodeling and functionality of immune cells.International journal of biological sciences · 2021Review
- Biological characteristics of transcription factor RelB in different immune cell types: implications for the treatment of multiple sclerosis.Molecular brain · 2019Review
- PD-L1- and calcitriol-dependent liposomal antigen-specific regulation of systemic inflammatory autoimmune disease.JCI insight · 2019Article
- Malnutrition: Modulator of Immune Responses in Tuberculosis.Frontiers in immunology · 2017Review
- Extraskeletal actions of vitamin D.Annals of the New York Academy of Sciences · 2016Review
- Metabolism Is Central to Tolerogenic Dendritic Cell Function.Mediators of inflammation · 2016Review
- Inflammation and Nutritional Science for Programs/Policies and Interpretation of Research Evidence (INSPIRE).The Journal of nutrition · 2015Review
- Dendritic cells and the promise of antigen-specific therapy in rheumatoid arthritis.Arthritis research & therapy · 2013Review
- Hypovitaminosis D as predisposing factor for atrophic type A gastritis: a case-control study and review of the literature on the interaction of Vitamin D with the immune system.Clinical reviews in allergy & immunology · 2012Article
- Role of vitamin D in insulin resistance.Journal of biomedicine & biotechnology · 2012Review
- MFG-E8 regulates the immunogenic potential of dendritic cells primed with necrotic cell-mediated inflammatory signals.PloS one · 2012Article
- Is multiple sclerosis an autoimmune disease?Autoimmune diseases · 2012Article
- Vitamin D3: a helpful immuno-modulator.Immunology · 2011Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The NF-kappaB component RelB is essential for dendritic cell (DC) differentiation and maturation. The vitamin D receptor (VDR) is a nuclear receptor that mediates inhibition of DC maturation and transcriptional repression of relB after engagement of its ligand, 1alpha,25-dihydroxyvitamin D(3), or related analogs (D(3) analogs). Ligand-dependent relB suppression was abolished by a histone deacetylase (HDAC) inhibitor. Constitutive association of VDR with the relB promoter was demonstrated in DCs by chromatin immunoprecipitation. Promoter binding by VDR was enhanced by ligand and reduced by LPS. Association of HDAC3 and HDAC1 with the relB VDR-binding site was observed, but only HDAC3 was reciprocally modulated by D(3) analog and LPS. Overexpression of HDAC3 caused relB promoter suppression, increased sensitivity to D(3) analog, and resistance to LPS. Depletion of HDAC3 attenuated relB suppression by D(3) analog. In vivo, D(3) analog resulted in reduced RelB in DCs from VDR WT mice but not VDR knockout mice. Other NF-lation of RelB and c-Rel in control animals. We conclude that vitamin D-regulated relB transcription in DCs is controlled by chromatin remodeling by means of recruitment of complexes including HDAC3.
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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.