ArticleJournal of virology2006
Rotavirus Nonstructural Protein NSP3 is not required for viral protein synthesis.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 87 citations in OpenAlex.
- Nucleolin-RNA interaction modulates rotavirus replication.Journal of virology · 2024Article
- Mature Rotavirus Particles Contain Equivalent Amounts ofJournal of virology · 2022Article
- Rotavirus Spike Protein VP4 Mediates Viroplasm Assembly by Association to Actin Filaments.Journal of virology · 2022Article
- Re-Examining Rotavirus Innate Immune Evasion: Potential Applications of the Reverse Genetics System.mBio · 2022Review
- Using Species a Rotavirus Reverse Genetics to Engineer Chimeric Viruses Expressing SARS-CoV-2 Spike Epitopes.Journal of virology · 2022Article
- Sneaking into the viral safe-houses: Implications of host components in regulating integrity and dynamics of rotaviral replication factories.Frontiers in cellular and infection microbiology · 2022Review
- Treading a HOSTile path: Mapping the dynamic landscape of host cell-rotavirus interactions to explore novel host-directed curative dimensions.Virulence · 2021Review
- Article
- Progressive Rotavirus Infection Downregulates Redox-Sensitive Transcription Factor Nrf2 and Nrf2-Driven Transcription Units.Oxidative medicine and cellular longevity · 2020Article
- Generation of Recombinant Rotavirus Expressing NSP3-UnaG Fusion Protein by a Simplified Reverse Genetics System.Journal of virology · 2019Article
- The Eukaryotic Translation Initiation Factor 4F Complex Restricts Rotavirus Infection via Regulating the Expression of IRF1 and IRF7.International journal of molecular sciences · 2019Article
- Rotavirus Infection Alters Splicing of the Stress-Related Transcription Factor XBP1.Journal of virology · 2019Article
- Selective inhibition of host cell signaling for rotavirus antivirals: PI3K/Akt/mTOR-mediated rotavirus pathogenesis.Virulence · 2018Article
- Rotavirus replication is correlated with S/G2 interphase arrest of the host cell cycle.PloS one · 2017Article
- Review
- Inflammatory and oxidative stress in rotavirus infection.World journal of virology · 2016Review
- Linking Α to Ω: diverse and dynamic RNA-based mechanisms to regulate gene expression by 5'-to-3' communication.F1000Research · 2016Review
- An Inhibitory Motif on the 5'UTR of Several Rotavirus Genome Segments Affects Protein Expression and Reverse Genetics Strategies.PloS one · 2016Article
- Challenging the Roles of NSP3 and Untranslated Regions in Rotavirus mRNA Translation.PloS one · 2016Article
- Rotavirus NSP3 Is a Translational Surrogate of the Poly(A) Binding Protein-Poly(A) Complex.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Initiation is the rate-limiting step in protein synthesis and therefore an important target for regulation. For the initiation of translation of most cellular mRNAs, the cap structure at the 5' end is bound by the translation factor eukaryotic initiation factor 4E (eIF4E), while the poly(A) tail, at the 3' end, is recognized by the poly(A)-binding protein (PABP). eIF4G is a scaffold protein that brings together eIF4E and PABP, causing the circularization of the mRNA that is thought to be important for an efficient initiation of translation. Early in infection, rotaviruses take over the host translation machinery, causing a severe shutoff of cell protein synthesis. Rotavirus mRNAs lack a poly(A) tail but have instead a consensus sequence at their 3' ends that is bound by the viral nonstructural protein NSP3, which also interacts with eIF4GI, using the same region employed by PABP. It is widely believed that these interactions lead to the translation of rotaviral mRNAs, impairing at the same time the translation of cellular mRNAs. In this work, the expression of NSP3 in infected cells was knocked down using RNA interference. Unexpectedly, under these conditions the synthesis of viral proteins was not decreased, while the cellular protein synthesis was restored. Also, the yield of viral progeny increased, which correlated with an increased synthesis of viral RNA. Silencing the expression of eIF4GI further confirmed that the interaction between eIF4GI and NSP3 is not required for viral protein synthesis. These results indicate that NSP3 is neither required for the translation of viral mRNAs nor essential for virus replication in cell culture.
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