ArticleJournal of virology2018
Partial Inactivation of the Chromatin Remodelers SMARCA2 and SMARCA4 in Virus-Infected Cells by Caspase-Mediated Cleavage.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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
9 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Secondary analysis of influenza a virus-infected cells at single-cell resolution reveals host BANF1 response to individual and combinations of detected segments.Virology journal · 2026Article
- Creation of a Novel Coding Program to Identify Genes Controlled by miRNAs During Human Rhinovirus Infection.Methods and protocols · 2025Article
- Chromatin Reorganization during Myoblast Differentiation Involves the Caspase-Dependent Removal of SATB2.Cells · 2022Article
- Cross-species analysis of viral nucleic acid interacting proteins identifies TAOKs as innate immune regulators.Nature communications · 2021Article
- Genome wide association study of passive immunity and disease traits in beef-suckler and dairy calves on Irish farms.Scientific reports · 2020Article
- AATF and SMARCA2 are associated with thyroid volume in Hashimoto's thyroiditis patients.Scientific reports · 2020Article
- A non-death function of the mitochondrial apoptosis apparatus in immunity.The EMBO journal · 2019Article
- Insights into bioinformatic approaches for repurposing compounds as anti-viral drugs.Antiviral chemistry & chemotherapyArticle
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The BAF-chromatin remodeling complex, with its mutually exclusive ATPases SMARCA2 and SMARCA4, is essential for the transcriptional activation of numerous genes, including a subset of interferon-stimulated genes (ISGs). Here, we show that C-terminally truncated forms of both SMARCA2 and SMARCA4 accumulate in cells infected with different RNA or DNA viruses. The levels of truncated SMARCA2 or SMARCA4 strongly correlate with the degree of cell damage and death observed after virus infection. The use of a pan-caspase inhibitor and genetically modified cell lines unable to undergo apoptosis revealed that the truncated forms result from the activity of caspases downstream of the activated intrinsic apoptotic pathway. C-terminally cleaved SMARCA2 and SMARCA4 lack potential nuclear localization signals as well as the bromo- and SnAC domain, with the latter two domains believed to be essential for chromatin association and remodeling. Consistent with this belief, C-terminally truncated SMARCA2 was partially relocated to the cytoplasm. However, the remaining nuclear protein was sufficient to induce ISG expression and inhibit the replication of vesicular stomatitis virus and influenza A virus. This suggests that virus-induced apoptosis does not occur at the expense of an intact interferon-mediated antiviral response pathway.
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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.