ArticleGenome research2015
Acute TNF-induced repression of cell identity genes is mediated by NFκB-directed redistribution of cofactors from super-enhancers.
Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 86 citations in OpenAlex.
- Single nucleus multiomics reveals an early inflammatory response to high-fat diet in mouse islets.Life science alliance · 2026Article
- Dynamic, anthracycline-induced chromatin alterations enable ALDH1 expression as a mechanism of inducible leukemia resistance development.Blood research · 2026Article
- Bromodomain-containing protein 4 in inflammatory diseases: molecular mechanisms and therapeutic potential.Journal of inflammation (London, England) · 2026Review
- Epromoters bind key stress-related transcription factors to regulate clusters of stress response genes.The EMBO journal · 2026Article
- Evaluation and Aggregation of Active Module Identification Algorithms.bioRxiv : the preprint server for biology · 2025Article
- Multi-species analysis of inflammatory response elements reveals ancient and lineage-specific contributions of transposable elements to NF-kB binding.Genome research · 2025Article
- Mutant CEBPA promotes tolerance to inflammatory stress through deficient AP-1 activation.Nature communications · 2025Article
- A Gremlin 1-expressing splenic niche cell population restrains chronic myeloid leukemia by antagonizing the BMP pathway.Nature cancer · 2025Article
- RBM43 controls PGC1α translation and a PGC1α-STING signaling axis.Cell metabolism · 2025Article
- ZNF143 binds DNA and stimulates transcription initiation to activate and repress direct target genes.Nucleic acids research · 2025Article
- Super-enhancers in immune system regulation: mechanisms, pathological reprogramming, and therapeutic opportunities.Frontiers in immunology · 2025Review
- IL-1β promotes adipogenesis by directly targeting adipocyte precursors.Nature communications · 2024Article
- Super-enhancer omics in stem cell.Molecular cancer · 2024Review
- ZNF143 binds DNA and stimulates transcripstion initiation to activate and repress direct target genes.bioRxiv : the preprint server for biology · 2024Article
- Super-Enhancers and Their Parts: From Prediction Efforts to Pathognomonic Status.International journal of molecular sciences · 2024Review
- Transcriptional and epigenomic profiling identifies YAP signaling as a key regulator of intestinal epithelium maturation.Science advances · 2023Article
- Review
- Bromodomain-containing protein 4 (BRD4): a key player in inflammatory bowel disease and potential to inspire epigenetic therapeutics.Expert opinion on therapeutic targets · 2023Review
- A local tumor microenvironment acquired super-enhancer induces an oncogenic driver in colorectal carcinoma.Nature communications · 2022Article
- Using iRNA-seq analysis to predict gene expression regulatory level and activity in Zea mays tissues.G3 (Bethesda, Md.) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proinflammatory cytokine tumor necrosis factor (TNF) plays a central role in low-grade adipose tissue inflammation and development of insulin resistance during obesity. In this context, nuclear factor κ-light-chain-enhancer of activated B cells (NFκB) is directly involved and required for the acute activation of the inflammatory gene program. Here, we show that the major transactivating subunit of NFκB, v-rel avian reticuloendotheliosis viral oncogene homolog A (RELA), is also required for acute TNF-induced suppression of adipocyte genes. Notably, this repression does not involve RELA binding to the associated enhancers but rather loss of cofactors and enhancer RNA (eRNA) selectively from high-occupancy sites within super-enhancers. Based on these data, we have developed models that, with high accuracy, predict which enhancers and genes are repressed by TNF in adipocytes. We show that these models are applicable to other cell types where TNF represses genes associated with super-enhancers in a highly cell-type-specific manner. Our results propose a novel paradigm for NFκB-mediated repression, whereby NFκB selectively redistributes cofactors from high-occupancy enhancers, thereby specifically repressing super-enhancer-associated cell identity genes.
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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.