ArticlePLoS biology2009
Two modes of transcriptional activation at native promoters by NF-kappaB p65.
Article in PLoS biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 78 citations in OpenAlex.
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- Role of PBAF and Mediator kinase module in the RELA-dependent activation ofFrontiers in immunology · 2026Article
- Single-cell RNA sequencing profiles age-related transcriptional landscapes in human hair follicle cells.hLife · 2025Article
- A Novel Effect of Id2 in Microglia TNFα Regulation.Molecular neurobiology · 2025Article
- Dihydrotestosterone Enhances MICA-Mediated Immune Responses to Epstein-Barr Virus-Associated Gastric Carcinoma.Cancers · 2024Article
- Transient interactions modulate the affinity of NF-κB transcription factors for DNA.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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- CRISPR/dCas-mediated gene activation toolkit development and its application for parthenogenesis induction in maize.Plant communications · 2023Article
- Enhancement of Vivid-based photo-activatable Gal4 transcription factor in mammalian cells.Cell structure and function · 2023Article
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- A transcriptional cycling model recapitulates chromatin-dependent features of noisy inducible transcription.PLoS computational biology · 2022Article
- A Dual Role for Cysteinyl Leukotriene Receptors in the Pathogenesis of Corneal Infection.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Review
- The cell polarity kinase Par1b/MARK2 activation selects specific NF-kB transcripts via phosphorylation of core mediator Med17/TRAP80.Molecular biology of the cell · 2021Article
- Global Transcriptomics Uncovers Distinct Contributions From Splicing Regulatory Proteins to the Macrophage Innate Immune Response.Frontiers in immunology · 2021Article
- Loss of Function Genetic Screen Identifies ATM Kinase as a Positive Regulator of TLR3-Mediated NF-κB Activation.iScience · 2020Article
- Role of cell-type specific nucleosome positioning in inducible activation of mammalian promoters.Nature communications · 2020Article
- Dissecting the Regulatory Strategies of NF-κB RelA Target Genes in the Inflammatory Response Reveals Differential Transactivation Logics.Cell reports · 2020Article
- A Novel Combined Scientific and Artistic Approach for the Advanced Characterization of Interactomes: The Akirin/Subolesin Model.Vaccines · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NF-kappaB family of transcription factors is crucial for the expression of multiple genes involved in cell survival, proliferation, differentiation, and inflammation. The molecular basis by which NF-kappaB activates endogenous promoters is largely unknown, but it seems likely that it should include the means to tailor transcriptional output to match the wide functional range of its target genes. To dissect NF-kappaB-driven transcription at native promoters, we disrupted the interaction between NF-kappaB p65 and the Mediator complex. We found that expression of many endogenous NF-kappaB target genes depends on direct contact between p65 and Mediator, and that this occurs through the Trap-80 subunit and the TA1 and TA2 regions of p65. Unexpectedly, however, a subset of p65-dependent genes are transcribed normally even when the interaction of p65 with Mediator is abolished. Moreover, a mutant form of p65 lacking all transcription activation domains previously identified in vitro can still activate such promoters in vivo. We found that without p65, native NF-kappaB target promoters cannot be bound by secondary transcription factors. Artificial recruitment of a secondary transcription factor was able to restore transcription of an otherwise NF-kappaB-dependent target gene in the absence of p65, showing that the control of promoter occupancy constitutes a second, independent mode of transcriptional activation by p65. This mode enables a subset of promoters to utilize a wide choice of transcription factors, with the potential to regulate their expression accordingly, whilst remaining dependent for their activation on NF-kappaB.
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