ArticleCell reports2015
Cooperative Transcriptional Activation of Antimicrobial Genes by STAT and NF-κB Pathways by Concerted Recruitment of the Mediator Complex.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 66 citations in OpenAlex.
- IFNγ shapes macrophage inflammatory responses by STAT1 isoform-specific epigenetic and transcriptional mechanisms.BMC genomics · 2026Article
- Enhanced hybridization-proximity labeling discovers protein interactomes of single RNA molecules.Nature communications · 2025Article
- STAT Signature Dish: Serving Immunity with a Side of Dietary Control.Biomolecules · 2025Review
- An evolutionarily conserved constellation of functional cis-elements programs the virus-responsive fate of the human (epi)genome.Nucleic acids research · 2025Article
- Linking signal input, cell state, and spatial context to inflammatory responses.Current opinion in immunology · 2024Review
- Transcriptional control of interferon-stimulated genes.The Journal of biological chemistry · 2024Review
- Threonine phosphorylation of STAT1 restricts interferon signaling and promotes innate inflammatory responses.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of ALEKSIN as a novel multi-IRF inhibitor of IRF- and STAT-mediated transcription in vascular inflammation and atherosclerosis.Frontiers in pharmacology · 2024Article
- CDK8 inhibitors antagonize HIV-1 reactivation and promote provirus latency in T cells.Journal of virology · 2023Article
- Adenosine receptor A2b confers ovarian cancer survival and PARP inhibitor resistance through IL-6-STAT3 signalling.Journal of cellular and molecular medicine · 2023Article
- Targeting the NF-κB pathway enhances responsiveness of mammary tumors to JAK inhibitors.Scientific reports · 2023Article
- CDK9 inhibition induces epigenetic reprogramming revealing strategies to circumvent resistance in lymphoma.Molecular cancer · 2023Article
- Case report: OccultFrontiers in medicine · 2023Article
- Stress signaling boosts interferon-induced gene transcription in macrophages.Science signaling · 2022Article
- Aligned electrospun poly(L-lactide) nanofibers facilitate wound healing by inhibiting macrophage M1 polarization via the JAK-STAT and NF-κB pathways.Journal of nanobiotechnology · 2022Article
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- Interferon stimulated binding of ISRE is cell type specific and is predicted by homeostatic chromatin state.Cytokine: X · 2021Article
- Disrupting interferon-alpha and NF-kappaB crosstalk suppresses IFITM1 expression attenuating triple-negative breast cancer progression.Cancer letters · 2021Article
- The role of macrophage polarization and associated mechanisms in regulating the anti-inflammatory action of acupuncture: a literature review and perspectives.Chinese medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional response to infection with the bacterium Listeria monocytogenes (Lm) requires cooperative signals of the type I interferon (IFN-I)-stimulated JAK-STAT and proinflammatory NF-κB pathways. Using ChIP-seq analysis, we define genes induced in Lm-infected macrophages through synergistic transcriptional activation by NF-κB and the IFN-I-activated transcription factor ISGF3. Using the Nos2 and IL6 genes as prime examples of this group, we show that NF-κB functions to recruit enzymes that establish histone marks of transcriptionally active genes. In addition, NF-κB regulates transcriptional elongation by employing the mediator kinase module for the recruitment of the pTEFb complex. ISGF3 has a major role in associating the core mediator with the transcription start as a prerequisite for TFIID and RNA polymerase II (Pol II) binding. Our data suggest that the functional cooperation between two major antimicrobial pathways is based on promoter priming by NF-κB and the engagement of the core mediator for Pol II binding by ISGF3.
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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.