Posttranscriptional Regulation of US11 in Cells Infected with a Herpes Simplex Virus 1 Recombinant Lacking Both 222-bp Domains Containing S-Component Origins of DNA Synthesis
Author:
Publisher
Elsevier BV
Subject
Virology
Reference52 articles.
1. Application of antibody to synthetic peptides for characterization of the intact and truncated α22 protein specified by herpes simplex virus 1 and the R325 α22− deletion mutant;Ackermann;J. Virol.,1985
2. Alternatively spliced mRNAs predicted to yield frame-shift proteins and stable intron 1 RNAs of the herpes simplex virus 1 regulatory gene α0 accumulate in the cytoplasm of infected cells;Carter;Proc. Natl. Acad. Sci. USA,1996
3. The second-site mutation in the herpes simplex virus recombinants lacking the γ134.5 genes precludes shutoff of protein synthesis by blocking the phosphorylation of eFI-2α;Cassady;J. Virol.,1998
4. The herpes simplex virus US11 protein effectively compensates for the γ134.5 gene if present before activation of protein kinase R by precluding its phosphorylation and that of the α subunit of eukaryotic translation initiation factor 2;Cassady;J. Virol.,1998
5. Animal virus DNA replication;Challberg;Ann. Rev. Biochem.,1989
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