ArticleJournal of virology2003
Identification of a lytic-cycle Epstein-Barr virus gene product that can regulate PKR activation.
Article in Journal of virology, 2003. 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
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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
33 citing papers in PubMed, 62 citations in OpenAlex.
- RNA recognition by PKR during DNA virus infection.Journal of medical virology · 2024Review
- Review
- Mechanism of herpesvirus protein kinase UL13 in immune escape and viral replication.Frontiers in immunology · 2022Review
- The herpesvirus accessory protein γ134.5 facilitates viral replication by disabling mitochondrial translocation of RIG-I.PLoS pathogens · 2021Article
- Inhibition of PKR by Viruses.Frontiers in microbiology · 2021Review
- Emerging translation strategies during virus-host interaction.Wiley interdisciplinary reviews. RNA · 2021Review
- Quantitative Proteomics Analysis of Lytic KSHV Infection in Human Endothelial Cells Reveals Targets of Viral Immune Modulation.Cell reports · 2020Article
- The integrated stress response in pulmonary disease.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Vaccinia Virus as a Master of Host Shutoff Induction: Targeting Processes of the Central Dogma and Beyond.Pathogens (Basel, Switzerland) · 2020Review
- Current Approaches for Combination Therapy of Cancer: The Role of Immunogenic Cell Death.Cancers · 2020Review
- The Immunomodulatory Capacity of an Epstein-Barr Virus Abortive Lytic Cycle: Potential Contribution to Viral Tumorigenesis.Cancers · 2018Review
- KSHV inhibits stress granule formation by viral ORF57 blocking PKR activation.PLoS pathogens · 2017Article
- Human Herpesvirus 6A Exhibits Restrictive Propagation with Limited Activation of the Protein Kinase R-eIF2α Stress Pathway.Journal of virology · 2017Article
- Modulation of the Translational Landscape During Herpesvirus Infection.Annual review of virology · 2015Review
- Herpesvirus-encoded GPCRs: neglected players in inflammatory and proliferative diseases?Nature reviews. Drug discovery · 2014Review
- Antagonism of the protein kinase R pathway by the guinea pig cytomegalovirus US22-family gene gp145.Virology · 2012Article
- Rapamycin-resistant mTORC1 kinase activity is required for herpesvirus replication.Journal of virology · 2010Article
- Tipping the balance: antagonism of PKR kinase and ADAR1 deaminase functions by virus gene products.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2009Review
- Autophagy as an emerging dimension to adaptive and innate immunity.Seminars in immunology · 2009Review
- Viral strategies to subvert the mammalian translation machinery.Progress in molecular biology and translational science · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Epstein-Barr virus (EBV) SM protein is a posttranscriptional regulator of viral gene expression. Like many transactivators encoded by herpesviruses, SM transports predominantly unspliced viral mRNA cargo from the nucleus to the cytosol, where it is subsequently translated. This activity likely involves a region of the protein that has homology to the herpes simplex virus type 1 (HSV-1) ICP27 gene product, the first member of this class of regulators to be discovered. However, SM also contains a repetitive segment rich in arginine and proline residues that is dispensable for its effects on RNA transport and splicing. This portion of SM, comprised of RXP triplet repeats, shows homology to the carboxyl-terminal domain of Us11, a double-stranded RNA (dsRNA) binding protein encoded by HSV-1 that inhibits activation of the cellular PKR kinase. To evaluate the intrinsic ability of SM to regulate PKR, we expressed and purified several SM protein derivatives and examined their activity in a variety of biochemical assays. The full-length SM protein bound dsRNA, associated physically with PKR, and prevented PKR activation. Removal of the 37-residue RXP domain significantly compromised all of these activities. Furthermore, the SM RXP domain was itself sufficient to inhibit PKR activation and interact with the kinase. Relative to its Us11 counterpart, the SM RXP segment bound dsRNA with reduced affinity and responded differently to single-stranded competitor polynucleotides. Thus, SM represents the first EBV gene product expressed during the lytic cycle that can prevent PKR activation. In addition, the RXP repeat segment appears to be a conserved herpesvirus motif capable of associating with dsRNA and modulating activation of the PKR kinase, a molecule important for the control of translation and the cellular antiviral response.
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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.