ArticleScientific reports2019
Bromodomain inhibitor JQ1 reversibly blocks IFN-γ production.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Bridging BET bromodomain and immune checkpoint inhibitors through generative bioorganic frameworks for next-generation cancer immunotherapy.RSC medicinal chemistry · 2026Review
- Epigenetic reprogramming of T cell metabolism restores function and enhances anti-tumor immunity in lung cancer.Nature immunology · 2026Article
- BET bromodomain inhibition potentiates antitumor activity of tumor-associated macrophages and enhances anti-CD47 immunotherapy in triple-negative breast cancer.Apoptosis : an international journal on programmed cell death · 2026Article
- Bromodomain and extra-terminal protein inhibitors modulate natural killer cell function and differentiation.Scientific reports · 2026Article
- [Inhibition of BRD4 promotes migration of esophageal squamous cell carcinoma cells with low ACC1 expression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Epigenetic Modifications in Osteosarcoma: Mechanisms and Therapeutic Strategies.Life (Basel, Switzerland) · 2025Review
- Super-enhancers in immune system regulation: mechanisms, pathological reprogramming, and therapeutic opportunities.Frontiers in immunology · 2025Review
- A human Tau expressing zebrafish model of progressive supranuclear palsy identifies Brd4 as a regulator of microglial synaptic elimination.Nature communications · 2024Article
- BET inhibitors drive Natural Killer activation in non-small cell lung cancer via BRD4 and SMAD3.Nature communications · 2024Article
- Effects of epigenetic therapy on natural killer cell function and development in hematologic malignancy.Journal of leukocyte biology · 2023Review
- Review
- Epigenetic remodeling of the immune landscape in cancer: therapeutic hurdles and opportunities.Journal of biomedical science · 2023Review
- Bromodomain-containing protein 4 (BRD4): a key player in inflammatory bowel disease and potential to inspire epigenetic therapeutics.Expert opinion on therapeutic targets · 2023Review
- Article
- Landscape of immune-related signatures induced by targeting of different epigenetic regulators in melanoma: implications for immunotherapy.Journal of experimental & clinical cancer research : CR · 2022Article
- Article
- Understanding the epigenetic mechanisms in SARS CoV-2 infection and potential therapeutic approaches.Virus research · 2022Review
- Epigenetics of alcohol-related liver diseases.JHEP reports : innovation in hepatology · 2022Review
- Article
- An in silico analysis identifies drugs potentially modulating the cytokine storm triggered by SARS-CoV-2 infection.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
As a class, 'BET' inhibitors disrupt binding of bromodomain and extra-terminal motif (BET) proteins, BRD2, BRD3, BRD4 and BRDT, to acetylated histones preventing recruitment of RNA polymerase 2 to enhancers and promoters, especially super-enhancers, to inhibit gene transcription. As such, BET inhibitors may be useful therapeutics for treatment of cancer and inflammatory disease. For example, the small molecule BET inhibitor, JQ1, selectively represses MYC, an important oncogene regulated by a super-enhancer. IFN-γ, a critical cytokine for both innate and adaptive immune responses, is also regulated by a super-enhancer. Here, we show that JQ1 represses IFN-γ expression in TH1 polarized PBMC cultures, CD4+ memory T cells, and NK cells. JQ1 treatment does not reduce activating chromatin marks at the IFNG locus, but displaces RNA polymerase II from the locus. Further, IFN-γ expression recovers in polarized TH1 cultures following removal of JQ1. Our results show that JQ1 abrogates IFN-γ expression, but repression is reversible. Thus, BET inhibitors may disrupt the normal functions of the innate and adaptive immune response.
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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.