ArticleiScience2018
Histone H2A.Z Suppression of Interferon-Stimulated Transcription and Antiviral Immunity Is Modulated by GCN5 and BRD2.
Article in iScience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- H2A.J is an epigenetic driver of IL-17-associated inflammation in TMolecular biomedicine · 2026Article
- Unraveling the layers of epigenetic control in respiratory antiviral defense.Journal of virology · 2026Review
- Human herpesvirus 6B U65 binds to histone proteins and suppresses interferon production.Journal of virology · 2025Article
- Histone variants: key regulators of inflammation in cell dedifferentiation and transdifferentiation.Frontiers in immunology · 2025Review
- Transcriptional control of interferon-stimulated genes.The Journal of biological chemistry · 2024Review
- Synergistic collaboration between AMPs and non-direct antimicrobial cationic peptides.Nature communications · 2024Article
- Article
- Dynamic control of gene expression by ISGF3 and IRF1 during IFNβ and IFNγ signaling.The EMBO journal · 2024Article
- Estrogen receptor α-mediated signaling inhibits type I interferon response to promote breast carcinogenesis.Journal of molecular cell biology · 2024Article
- RNA-Seq Analysis of Trans-Differentiated ARPE-19 Cells Transduced by AAV9-AIPL1 Vectors.International journal of molecular sciences · 2023Article
- Do plant histone variants stand idly by while DNA viruses invade the nucleus?Stress biology · 2023Article
- Competition for H2A.Z underlies the developmental impacts of repetitive element de-repression.Development (Cambridge, England) · 2023Article
- Next-generation bromodomain inhibitors of the SWI/SNF complex enhance DNA damage and cell death in glioblastoma.Journal of cellular and molecular medicine · 2023Article
- Mutation of Basic Residues R283, R286, and K288 in the Matrix Protein of Newcastle Disease Virus Attenuates Viral Replication and Pathogenicity.International journal of molecular sciences · 2023Article
- Stress signaling boosts interferon-induced gene transcription in macrophages.Science signaling · 2022Article
- Article
- The TRRAP transcription cofactor represses interferon-stimulated genes in colorectal cancer cells.eLife · 2022Article
- Myeloid cell nuclear differentiation antigen controls the pathogen-stimulated type I interferon cascade in human monocytes by transcriptional regulation of IRF7.Nature communications · 2022Article
- BRD2 inhibition blocks SARS-CoV-2 infection by reducing transcription of the host cell receptor ACE2.Nature cell biology · 2022Article
- Interferon stimulated binding of ISRE is cell type specific and is predicted by homeostatic chromatin state.Cytokine: X · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Type I interferon (IFN)-stimulated gene (ISG) expression requires interaction between a transcription factor complex, ISGF3, and target gene promoters to initiate transcription and protection against infection. To uncover chromatin regulatory features of this antiviral immune response, IFN-induced nucleosome and histone dynamics of human ISG loci were examined. ISGF3 recruitment after IFN stimulation was accompanied by nucleosome reorganization at promoters and gene bodies. IFN stimulation induced loss of core histones H2B, H3, and H4, as well as H2A.Z at ISG promoters. A strong correlation was found between H2A.Z occupancy and ISGF3 target sites, and IFN-stimulated H2A.Z removal requires STAT1, STAT2, and IRF9. Neither INO80 nor SWI/SNF participate in IFN-driven H2A.Z eviction, but GCN5 and BRD2 are required. Interference with H2A.Z expression enhanced ISGF3 recruitment to ISG promoters, ISG mRNA expression, and IFN-stimulated antiviral immunity. This indicates that H2A.Z nucleosomes at ISG promoters restrict optimal ISGF3 engagement and modulate the biological response to IFN.
Indexed as
Identifiers
What OpenQuestion holds
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.