ArticleJournal of virology2008
Epstein-Barr virus SM protein functions as an alternative splicing factor.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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.
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Who cites it
43 citing papers in PubMed, 60 citations in OpenAlex.
- Overview on Epstein-Barr Virus-Host Interactions With a Focus on Host Cell Transcriptome Alterations.Cell biochemistry and function · 2026Review
- A BRRF1-CCR4-NOT axis underlies conserved transcriptome-wide loss of splicing fidelity during gammaherpesvirus reactivation.bioRxiv : the preprint server for biology · 2026Article
- Transcriptional and Alternative Splicing Regulation of Autophagy and Vesicle Transport Pathways in Large Yellow Croaker Cells During Megalocytivirus Infection.Animals : an open access journal from MDPI · 2026Article
- Macrophage Zc3h12c Limits Tissue Inflammation and Injury via Alternative Splicing of Pre-mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Viral Modulation of Host Splicing.Annual review of virology · 2025Review
- Epstein-Barr virus induces host shutoff extensively via BGLF5-independent mechanisms.Cell reports · 2024Article
- Variant- and vaccination-specific alternative splicing profiles in SARS-CoV-2 infections.iScience · 2024Article
- Variant- and Vaccination-Specific Alternative Splicing Profiles in SARS-CoV-2 Infections.bioRxiv : the preprint server for biology · 2023Article
- An Epstein-Barr virus protein interaction map reveals NLRP3 inflammasome evasion via MAVS UFMylation.Molecular cell · 2023Article
- Virus usurps alternative splicing to clear the decks for infection.Virology journal · 2023Review
- Contribution of Epstein-Barr Virus Lytic Proteins to Cancer Hallmarks and Implications from Other Oncoviruses.Cancers · 2023Review
- Epstein-Barr Virus Enhances Cancer-Specific Aberrant Splicing of TSG101 Pre-mRNA.International journal of molecular sciences · 2022Article
- Review
- Modulation of alternative splicing during early infection of human primary B lymphocytes with Epstein-Barr virus (EBV): a novel function for the viral EBNA-LP protein.Nucleic acids research · 2021Article
- Review
- Aberrant Splicing Events and Epigenetics in Viral Oncogenomics: Current Therapeutic Strategies.Cells · 2021Review
- Epstein-Barr virus co-opts TFIIH component XPB to specifically activate essential viral lytic promoters.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Circular RNAs: New Epigenetic Signatures in Viral Infections.Frontiers in microbiology · 2020Review
- Viral modulation of cellular RNA alternative splicing: A new key player in virus-host interactions?Wiley interdisciplinary reviews. RNA · 2019Review
- How Many Mammalian Reovirus Proteins are involved in the Control of the Interferon Response?Pathogens (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alternative splicing of RNA increases the coding potential of the genome and allows for additional regulatory control over gene expression. The full extent of alternative splicing remains to be defined but is likely to significantly expand the size of the human transcriptome. There are several examples of mammalian viruses regulating viral splicing or inhibiting cellular splicing in order to facilitate viral replication. Here, we describe a viral protein that induces alternative splicing of a cellular RNA transcript. Epstein-Barr virus (EBV) SM protein is a viral protein essential for replication that enhances EBV gene expression by enhancing RNA stability and export. SM also increases cellular STAT1 expression, a central mediator of interferon signal transduction, but disproportionately increases the abundance of the STAT1beta splicing isoform, which can act as a dominant-negative suppressor of STAT1alpha. SM induces splicing of STAT1 at a novel 5' splice site, resulting in a STAT1 mRNA incapable of producing STAT1alpha. SM-induced alternative splicing is dependent on the presence of an RNA sequence to which SM binds directly and which can confer SM-dependent splicing on heterologous RNA. The cellular splicing factor ASF/SF2 also binds to this region and inhibits SM-RNA binding and SM-induced alternative splicing. These results suggest that viruses may regulate cellular gene expression at the level of alternative mRNA splicing in order to facilitate virus replication or persistence in vivo.
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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.