Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
about
Mutations within the conserved NS1 nuclear export signal lead to inhibition of influenza A virus replicationInfluenza A virus attenuation by codon deoptimization of the NS gene for vaccine developmentViral factors in influenza pandemic risk assessment.Influenza A virus transmission bottlenecks are defined by infection route and recipient host.The "histone mimicry" by pathogens.Drosha as an interferon-independent antiviral factor.Recruitment of RED-SMU1 complex by Influenza A Virus RNA polymerase to control Viral mRNA splicingThe Mammalian response to virus infection is independent of small RNA silencing.Genome rearrangement of influenza virus for anti-viral drug screeningA GFP expressing influenza A virus to report in vivo tropism and protection by a matrix protein 2 ectodomain-specific monoclonal antibody.Influenza A Virus NS1 Protein Inhibits the NLRP3 Inflammasome.Generation of a variety of stable Influenza A reporter viruses by genetic engineering of the NS gene segment.Downregulating viral gene expression: codon usage bias manipulation for the generation of novel influenza A virus vaccines.An A14U Substitution in the 3' Noncoding Region of the M Segment of Viral RNA Supports Replication of Influenza Virus with an NS1 Deletion by Modulating Alternative Splicing of M Segment mRNAsIn Vivo RNAi Screening Identifies MDA5 as a Significant Contributor to the Cellular Defense against Influenza A VirusMolecular Determinants of Virulence and Stability of a Reporter-Expressing H5N1 Influenza A VirusAccurate Measurement of the Effects of All Amino-Acid Mutations on Influenza Hemagglutinin.MicroRNA-based strategy to mitigate the risk of gain-of-function influenza studies.Transport of the influenza virus genome from nucleus to nucleusA versatile RNA vector for delivery of coding and noncoding RNAs.An NS-segment exonic splicing enhancer regulates influenza A virus replication in mammalian cells.Biogenesis, assembly, and export of viral messenger ribonucleoproteins in the influenza A virus infected cell.Influenza viruses and mRNA splicing: doing more with lessDevelopment and applications of single-cycle infectious influenza A virus (sciIAV).MicroRNA-based Regulation of Picornavirus Tropism.Phosphorylation of highly conserved serine residues in the influenza A virus nuclear export protein NEP plays a minor role in viral growth in human cells and mice.Overcoming NS1-mediated immune antagonism involves both interferon-dependent and independent mechanismsmicroRNA-based attenuation of influenza virus across susceptible hosts.Extreme heterogeneity of influenza virus infection in single cells.
P2860
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P2860
Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
description
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Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
@en
Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
@nl
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Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
@en
Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
@nl
prefLabel
Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
@en
Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
@nl
P2093
P2860
P1433
P1476
Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection
@en
P2093
Benjamin R Tenoever
Jasmine T Perez
Mark A Chua
Ryan A Langlois
P2860
P356
10.1016/J.CELREP.2012.12.010
P50
P577
2013-01-17T00:00:00Z