ArticleJournal of cellular biochemistry2015
Transcriptional regulation of the human TNFSF11 gene in T cells via a cell type-selective set of distal enhancers.
Article in Journal of cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 39 citations in OpenAlex.
- The vitamin D receptor story: discovery, control, and genomic reach.The Journal of endocrinology · 2026Review
- Transcriptional regulation of Rankl by Txnip-Ecd in aging and diabetic related osteoporosis.Journal of advanced research · 2025Article
- Epigenetic Modifications of White Blood Cell DNA Caused by Transient Fetal Infection with Bovine Viral Diarrhea Virus.Viruses · 2024Article
- Osteomesopyknosis associated with a novel ALOX5 variant that impacts the RANKL pathway.Molecular genetics & genomic medicine · 2024Article
- Molecular Subtype Classification of Postmenopausal Osteoporosis and Immune Infiltration Microenvironment Based on Bioinformatics Analysis of Osteoclast-Regulatory Genes.Biomedicines · 2023Article
- Identification of an intronic enhancer regulating RANKL expression in osteocytic cells.Bone research · 2023Article
- Genomic mechanisms controlling renal vitamin D metabolism.The Journal of steroid biochemistry and molecular biology · 2023Article
- ETS1 governs pathological tissue-remodeling programs in disease-associated fibroblasts.Nature immunology · 2022Article
- Article
- Association ofBalkan journal of medical genetics : BJMG · 2021Article
- Supranutritional selenium suppresses ROS-induced generation of RANKL-expressing osteoclastogenic CD4Clinical & translational immunology · 2021Article
- The Transcriptional Differences of Avian CD4Frontiers in cellular and infection microbiology · 2021Article
- Article
- Article
- A Novel Distal Enhancer Mediates Inflammation-, PTH-, and Early Onset Murine Kidney Disease-Induced Expression of the MouseJBMR plus · 2018Article
- Parathyroid Hormone Signaling in Osteocytes.JBMR plus · 2018Review
- Deletion of a Distal RANKL Gene Enhancer Delays Progression of Atherosclerotic Plaque Calcification in Hypercholesterolemic Mice.Journal of cellular biochemistry · 2017Article
- Biology and Mechanisms of Action of the Vitamin D Hormone.Endocrinology and metabolism clinics of North America · 2017Review
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In addition to osteoblast lineage cells, the TNF-like factor receptor activator of NF-κB ligand (RANKL) is expressed in both B and T cells and may play a role in bone resorption. Rankl gene (Tnfsf11) expression in mouse T cells is mediated through multiple distal elements marked by increased transcription factor occupancy, histone tail acetylation, and RNA polymerase II recruitment. Little is known, however, of the regulation of human TNFSF11 in T cells. Accordingly, we examined the consequence of T cell activation on the expression of this factor both in Jurkat cells and in primary human T cells. We then explored the mechanism of this regulation by scanning over 400 kb of DNA surrounding the TNFSF11 locus for regulatory enhancers using ChIP-chip analysis. Histone H3/H4 acetylation enrichment identified putative regulatory regions located between -170 and -220 kb upstream of the human TNFSF11 TSS that we designated the human T cell control region (hTCCR). This region showed high sequence conservation with the mouse TCCR. Inhibition of MEK1/2 by U0126 resulted in decreased RANKL expression suggesting that stimulation through MEK1/2 was a prerequisite. ChIP-chip analysis also revealed that c-FOS was recruited to the hTCCR as well. Importantly, both the human TNFSF11 D5a/b (RLD5a/b) enhancer and segments of the hTCCR mediated robust inducible reporter activity following TCR activation. Finally, SNPs implicated in diseases characterized by dysregulated BMD co-localized to the hTCCR region. We conclude that the hTCCR region contains a cell-selective set of enhancers that plays an integral role in the transcriptional regulation of the TNFSF11 gene in human T cells.
Indexed as
Identifiers
What OpenQuestion holds
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.