Cellular mRNA translation is blocked at both initiation and elongation after infection by influenza virus or adenovirus
about
Specific residues of PB2 and PA influenza virus polymerase subunits confer the ability for RNA polymerase II degradation and virus pathogenicity in miceInfluenza A Virus Protein PA-X Contributes to Viral Growth and Suppression of the Host Antiviral and Immune ResponsesTwenty amino acids at the C-terminus of PA-X are associated with increased influenza A virus replication and pathogenicity.mRNAs encoding ribulose-1,5-bisphosphate carboxylase remain bound to polysomes but are not translated in amaranth seedlings transferred to darkness.RNase L-independent specific 28S rRNA cleavage in murine coronavirus-infected cellsGlobal impact of influenza virus on cellular pathways is mediated by both replication-dependent and -independent events.Protein synthesis shut-off induced by influenza virus infection is independent of PKR activityAdenovirus VAI RNA complexes with the 68 000 Mr protein kinase to regulate its autophosphorylation and activityTranslational control of viral gene expression in eukaryotesCap-independent translation of mRNA conferred by encephalomyocarditis virus 5' sequence improves the performance of the vaccinia virus/bacteriophage T7 hybrid expression systemSelective translation of eukaryotic mRNAs: functional molecular analysis of GRSF-1, a positive regulator of influenza virus protein synthesis.Monomeric scAlu and nascent dimeric Alu RNAs induced by adenovirus are assembled into SRP9/14-containing RNPs in HeLa cells.A comprehensive map of the influenza A virus replication cycleTranscriptome profiling of influenza A virus-infected lung epithelial (A549) cells with lariciresinol-4-β-D-glucopyranoside treatmentThe presence of tat protein or tumor necrosis factor alpha is critical for herpes simplex virus type 1-induced expression of human immunodeficiency virus type 1.Modification of eukaryotic initiation factor 4F during infection by influenza virus.Identification of the N-terminal domain of the influenza virus PA responsible for the suppression of host protein synthesis.Effect of mutations and deletions in a bicistronic mRNA on the synthesis of influenza B virus NB and NA glycoproteins.Characterization of the translational defect to fiber synthesis in monkey cells abortively infected with human adenovirus: role of ancillary leaders.Efficient transcription, not translation, is dependent on adenovirus tripartite leader sequences at late times of infection.Analysis of the transcript of the herpes simplex virus DNA polymerase gene provides evidence that polymerase expression is inefficient at the level of translation.Influenza virus regulates protein synthesis during infection by repressing autophosphorylation and activity of the cellular 68,000-Mr protein kinase.Downregulation of cell surface molecules during noncytopathic infection of T cells with human immunodeficiency virus.Defective RNA replication and late gene expression in temperature-sensitive influenza viruses expressing deleted forms of the NS1 proteinAttenuated strains of influenza A viruses do not induce degradation of RNA polymerase II.Influenza virus mRNA translation revisited: is the eIF4E cap-binding factor required for viral mRNA translation?CHD6, a cellular repressor of influenza virus replication, is degraded in human alveolar epithelial cells and mice lungs during infection.Eukaryotic translation initiation factor 4GI is a cellular target for NS1 protein, a translational activator of influenza virus.The N-terminal half of the influenza virus NS1 protein is sufficient for nuclear retention of mRNA and enhancement of viral mRNA translation.Adenovirus virus-associated RNAII-derived small RNAs are efficiently incorporated into the rna-induced silencing complex and associate with polyribosomes.Direct measurement of tubulin and bulk message distributions on polysomes of growing, starved and deciliated Tetrahymena using RNA gel blots of sucrose gradients containing acrylamide.A systematic view on influenza induced host shutoff.Inhibition of Influenza Virus Replication by DNA Aptamers Targeting a Cellular Component of Translation Initiation.Influenza virus polymerase confers independence of the cellular cap-binding factor eIF4E for viral mRNA translation.Comprehending a Killer: The Akt/mTOR Signaling Pathways Are Temporally High-Jacked by the Highly Pathogenic 1918 Influenza Virus.
P2860
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P2860
Cellular mRNA translation is blocked at both initiation and elongation after infection by influenza virus or adenovirus
description
1986 nî lūn-bûn
@nan
1986年の論文
@ja
1986年論文
@yue
1986年論文
@zh-hant
1986年論文
@zh-hk
1986年論文
@zh-mo
1986年論文
@zh-tw
1986年论文
@wuu
1986年论文
@zh
1986年论文
@zh-cn
name
Cellular mRNA translation is b ...... influenza virus or adenovirus
@en
type
label
Cellular mRNA translation is b ...... influenza virus or adenovirus
@en
prefLabel
Cellular mRNA translation is b ...... influenza virus or adenovirus
@en
P2093
P2860
P1433
P1476
Cellular mRNA translation is b ...... influenza virus or adenovirus
@en
P2093
P2860
P304
P407
P577
1986-12-01T00:00:00Z