ArticleMolecular and cellular biology2013
The human RVB complex is required for efficient transcription of type I interferon-stimulated genes.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Genome-scale perturbation signatures from primary human CD4bioRxiv : the preprint server for biology · 2026Article
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- Malignant JAK-signaling: at the interface of inflammation and malignant transformation.Leukemia · 2025Review
- Transcriptional control of interferon-stimulated genes.The Journal of biological chemistry · 2024Review
- Article
- Adenovirus E1A binding to DCAF10 targets proteasomal degradation of RUVBL1/2 AAA+ ATPases required for quaternary assembly of multiprotein machines, innate immunity, and responses to metabolic stress.Journal of virology · 2023Article
- African swine fever virus pA104R protein acts as a suppressor of type I interferon signaling.Frontiers in microbiology · 2023Article
- Review
- The transcriptional coactivator RUVBL2 regulates Pol II clustering with diverse transcription factors.Nature communications · 2022Article
- Article
- BRD9 is a druggable component of interferon-stimulated gene expression and antiviral activity.EMBO reports · 2021Article
- A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.Nature communications · 2019Article
- Nrf1-mediated transcriptional regulation of the proteasome requires a functional TIP60 complex.The Journal of biological chemistry · 2019Article
- HDAC stimulates gene expression through BRD4 availability in response to IFN and in interferonopathies.The Journal of experimental medicine · 2018Article
- Transcriptional and chromatin regulation in interferon and innate antiviral gene expression.Cytokine & growth factor reviews · 2018Review
- Histone H2A.Z Suppression of Interferon-Stimulated Transcription and Antiviral Immunity Is Modulated by GCN5 and BRD2.iScience · 2018Article
- Suppression of Type I Interferon Signaling by E1A via RuvBL1/Pontin.Journal of virology · 2017Article
- The Role of Pontin and Reptin in Cellular Physiology and Cancer Etiology.Frontiers in molecular biosciences · 2017Review
- Vaccinia Virus Protein C6 Inhibits Type I IFN Signalling in the Nucleus and Binds to the Transactivation Domain of STAT2.PLoS pathogens · 2016Article
- Phosphorylation of STAT2 on serine-734 negatively regulates the IFN-α-induced antiviral response.Journal of cell science · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Type I interferons (IFNs) stimulate transcription through a latent heterotrimeric transcription factor composed of tyrosine-phosphorylated STAT1 and STAT2 and the DNA binding partner IRF9, with STAT2 contributing a critical transactivation domain. Human RVB1 and RVB2, which are highly conserved AAA(+) ATP binding proteins contained in chromatin-remodeling complexes such as Ino80, SNF2-related CBP activator protein (SRCAP), and Tip60/NuA4, interacted with the transactivation domain of STAT2 in the nuclei of IFN-stimulated cells. RNA interference (RNAi) experiments demonstrated that RVB proteins were required for robust activation of IFN-α-stimulated genes (ISGs). The requirement for RVB proteins was specific to IFN-α/STAT2 signaling; transcription of tumor necrosis factor alpha (TNF-α)- and IFN-γ-driven genes was not affected by RVB1 depletion. Using RNAi-based depletion, we assessed the involvement of catalytic subunits of the RVB-containing Tip60, BRD8, Ino80, SRCAP, and URI complexes. No component other than RVB1/2 was uniquely required for ISG induction, suggesting that RVB1/2 functions as part of an as yet unidentified complex. Chromatin immunoprecipitation assays indicated that RVB1/2 was required for recruitment of RNA polymerase II (Pol II) to ISG promoters but was dispensable for STAT2 recruitment to chromatin. We hypothesize that an RVB1/2 chromatin-remodeling complex is required for efficient Pol II recruitment and initiation at ISG promoters and is recruited through interaction with the STAT2 transactivation domain.
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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.