ArticleProceedings of the National Academy of Sciences of the United States of America2022
BRD9 regulates interferon-stimulated genes during macrophage activation via cooperation with BET protein BRD4.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 46 citations in OpenAlex.
- Virtual screening and cellular validation of dolutegravir as a BRD9 inhibitor for attenuating pyroptosis in peritoneal mesothelial cells.Renal failure · 2026Article
- Tandem bromodomains of BRD4 cooperatively read poly-acetylated nucleosomes to enhance chromatin engagement and regulate breast cancer phenotypes.bioRxiv : the preprint server for biology · 2026Article
- Review
- Bromodomain-containing protein 4 in inflammatory diseases: molecular mechanisms and therapeutic potential.Journal of inflammation (London, England) · 2026Review
- Highly discriminative globin gene activation by the noncanonical BAF chromatin remodeling complex.Blood · 2026Article
- E3 ligase UHRF2 hijacks nuclear TBK1 to epigenetically repress type I interferons expression.International journal of biological sciences · 2026Article
- BRD9 at the crossroads of splicing, chromatin remodeling, and hematopoiesis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2026Review
- Identification of an IRF-ZBP1-caspase-8-NINJ1 axis in driving PANoptosis and pathology during alcohol-associated liver disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Article
- Control of Inflammatory Response by Tissue Microenvironment.bioRxiv : the preprint server for biology · 2025Article
- Mechanisms of Impaired Wound Healing in Type 2 Diabetes: The Role of Epigenetic Factors.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Brd9 antagonism induces beige adipocytes in white adipose tissues and protects against diet-induced obesity.Obesity (Silver Spring, Md.) · 2025Article
- Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.Epigenetics & chromatin · 2025Review
- A Recent Overview of Molecular Pathways in Synthetic Lethality as a Proposed Valid Target in Oncology: Current Insights and Future Directions.Indian journal of surgical oncology · 2025Review
- Chromatin remodeling in lymphocytic function and fate: the multifaceted roles of SWI/SNF complex.Frontiers in immunology · 2025Review
- Regulatory Roles of SWI/SNF Chromatin Remodeling Complexes in Immune Response and Inflammatory Diseases.Clinical reviews in allergy & immunology · 2024Review
- Programmed BRD9 Degradation and Hedgehog Signaling Activation via Silk-Based Core-Shell Microneedles Promote Diabetic Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024Review
- BRD9 promotes the progression of gallbladder cancer via CST1 upregulation and interaction with FOXP1 through the PI3K/AKT pathway and represents a therapeutic target.Gene therapy · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages induce a number of inflammatory response genes in response to stimulation with microbial ligands. In response to endotoxin Lipid A, a gene-activation cascade of primary followed by secondary-response genes is induced. Epigenetic state is an important regulator of the kinetics, specificity, and mechanism of gene activation of these two classes. In particular, SWI/SNF chromatin-remodeling complexes are required for the induction of secondary-response genes, but not primary-response genes, which generally exhibit open chromatin. Here, we show that a recently discovered variant of the SWI/SNF complex, the noncanonical BAF complex (ncBAF), regulates secondary-response genes in the interferon (IFN) response pathway. Inhibition of bromodomain-containing protein 9 (BRD9), a subunit of the ncBAF complex, with BRD9 bromodomain inhibitors (BRD9i) or a degrader (dBRD9) led to reduction in a number of interferon-stimulated genes (ISGs) following stimulation with endotoxin lipid A. BRD9-dependent genes overlapped highly with a subset of genes differentially regulated by BET protein inhibition with JQ1 following endotoxin stimulation. We find that the BET protein BRD4 is cobound with BRD9 in unstimulated macrophages and corecruited upon stimulation to ISG promoters along with STAT1, STAT2, and IRF9, components of the ISGF3 complex activated downstream of IFN-alpha receptor stimulation. In the presence of BRD9i or dBRD9, STAT1-, STAT2-, and IRF9-binding is reduced, in some cases with reduced binding of BRD4. These results demonstrate a specific role for BRD9 and the ncBAF complex in ISG activation and identify an activity for BRD9 inhibitors and degraders in dampening endotoxin- and IFN-dependent gene expression.
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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.