ArticleNucleic acids research2025
3D enhancer architecture coordinated by CTCF determines immune-related gene expression patterns via RNA polymerase II pause-release in CD4+ T cells.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- ATF4 and CHOP coordinate endoplasmic reticulum stress-responsive gene programs through enhancer activation and chromatin looping.Nucleic acids research · 2026Article
- Effect of Leaf Extracts of Cornus sanguinea L., C. sericea L., and C. alba L. on Digestive Enzymes and Blood Coagulation In Vitro.Plant foods for human nutrition (Dordrecht, Netherlands) · 2026Article
- Enhancers integrate microenvironmental signals in muscle stem cells during regeneration in health, disease, and aging.Skeletal muscle · 2026Review
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5 authors.
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Abstract
CTCF (CCCTC-binding factor) is crucial for organizing mammalian genomes into domains and structural loops, yet its role in enhancer-promoter interactions remains unclear. Here, we demonstrate that 3D enhancer architecture undergoes marked reorganization upon CTCF depletion in activated CD4+ T cells. Despite this, active transcription, particularly driven by STAT5-bound super-enhancers, maintains enhancer loops independently of CTCF. Interestingly, robust enhancer-promoter interactions are associated with the release of RNA polymerase II (RNAPII) pausing and require CTCF-dependent 3D genome organization to shape immune-related gene expression patterns in CD4+ T cells. Notably, CTCF depletion reprograms the transcriptional response of CD4+ T cells to JAK inhibitors by rewiring the STAT5 enhancer network rather than altering the upstream JAK/STAT signaling cascade. This study emphasizes the role of 3D enhancer architecture orchestrated by CTCF and active transcription in directing precise cell identity gene expression through RNAPII pause-release in CD4+ T cells.
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