ArticleEMBO reports2021
BRD9 is a druggable component of interferon-stimulated gene expression and antiviral activity.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Unraveling the layers of epigenetic control in respiratory antiviral defense.Journal of virology · 2026Review
- BRD9 inhibition overcomes oncolytic virus therapy resistance in glioblastoma.Cell reports. Medicine · 2025Article
- CRISPR with Transcriptional Readout reveals influenza transcription is modulated by NELF and can precipitate an interferon response.bioRxiv : the preprint server for biology · 2025Article
- BRD9 functions as an HIV-1 latency regulatory factor.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Brd9 antagonism induces beige adipocytes in white adipose tissues and protects against diet-induced obesity.Obesity (Silver Spring, Md.) · 2025Article
- An atlas of protein phosphorylation dynamics during interferon signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Systematic reconstruction of molecular pathway signatures using scalable single-cell perturbation screens.Nature cell biology · 2025Article
- Data-driven projections of candidate enhancer-activating SNPs in immune regulation.BMC genomics · 2025Article
- 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
- Article
- BRD9 regulates normal human hematopoietic stem cell function and lineage differentiation.Cell death and differentiation · 2024Article
- Proximal protein landscapes of the type I interferon signaling cascade reveal negative regulation by PJA2.Nature communications · 2024Article
- Article
- A genome-wide optical pooled screen reveals regulators of cellular antiviral responses.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- BRD9-mediated chromatin remodeling suppresses osteoclastogenesis through negative feedback mechanism.Nature communications · 2023Article
- Epigenetic and pharmacological control of pigmentation via Bromodomain Protein 9 (BRD9).Pigment cell & melanoma research · 2023Article
- Ultra-Rare BRD9 Loss-of-Function Variants Limit the Antiviral Action of Interferon.Scientific reports · 2022Article
- Restriction factor screening identifies RABGAP1L-mediated disruption of endocytosis as a host antiviral defense.Cell reports · 2022Article
- BRD9 regulates interferon-stimulated genes during macrophage activation via cooperation with BET protein BRD4.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN) induction of IFN-stimulated genes (ISGs) creates a formidable protective antiviral state. However, loss of appropriate control mechanisms can result in constitutive pathogenic ISG upregulation. Here, we used genome-scale loss-of-function screening to establish genes critical for IFN-induced transcription, identifying all expected members of the JAK-STAT signaling pathway and a previously unappreciated epigenetic reader, bromodomain-containing protein 9 (BRD9), the defining subunit of non-canonical BAF (ncBAF) chromatin-remodeling complexes. Genetic knockout or small-molecule-mediated degradation of BRD9 limits IFN-induced expression of a subset of ISGs in multiple cell types and prevents IFN from exerting full antiviral activity against several RNA and DNA viruses, including influenza virus, human immunodeficiency virus (HIV1), and herpes simplex virus (HSV1). Mechanistically, BRD9 acts at the level of transcription, and its IFN-triggered proximal association with the ISG transcriptional activator, STAT2, suggests a functional localization at selected ISG promoters. Furthermore, BRD9 relies on its intact acetyl-binding bromodomain and unique ncBAF scaffolding interaction with GLTSCR1/1L to promote IFN action. Given its druggability, BRD9 is an attractive target for dampening ISG expression under certain autoinflammatory conditions.
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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.