ArticleJournal of virology1998
The role of herpes simplex virus ICP27 in the regulation of UL24 gene expression by differential polyadenylation.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Comparative Review of the Conserved UL24 Protein Family in Herpesviruses.International journal of molecular sciences · 2024Review
- Suppression of HSV-1 infection and viral reactivation by CRISPR-Cas9 gene editing in 2D and 3D culture models.Molecular therapy. Nucleic acids · 2024Article
- Aberrant RNA polymerase initiation and processivity on the genome of a herpes simplex virus 1 mutant lacking ICP27.Journal of virology · 2024Article
- Mechanism of herpesvirus UL24 protein regulating viral immune escape and virulence.Frontiers in microbiology · 2023Review
- Integrative functional genomics decodes herpes simplex virus 1.Nature communications · 2020Article
- Minute Virus of Canines NP1 Protein Interacts with the Cellular Factor CPSF6 To Regulate Viral Alternative RNA Processing.Journal of virology · 2019Article
- Herpes simplex virus ICP27 regulates alternative pre-mRNA polyadenylation and splicing in a sequence-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- NP1 Protein of the Bocaparvovirus Minute Virus of Canines Controls Access to the Viral Capsid Genes via Its Role in RNA Processing.Journal of virology · 2016Article
- Duck enteritis virus UL54 is an IE protein primarily located in the nucleus.Virology journal · 2015Article
- Widespread disruption of host transcription termination in HSV-1 infection.Nature communications · 2015Article
- Construction and identification of a cDNA library for use in the yeast two-hybrid system from duck embryonic fibroblast cells post-infected with duck enteritis virus.Molecular biology reports · 2014Article
- Article
- Whole-genome analysis of pseudorabies virus gene expression by real-time quantitative RT-PCR assay.BMC genomics · 2009Article
- Herpes simplex virus type 1 infection leads to loss of serine-2 phosphorylation on the carboxyl-terminal domain of RNA polymerase II.Journal of virology · 2005Article
- Herpes simplex virus ICP27 activation of stress kinases JNK and p38.Journal of virology · 2005Article
- Role of the varicella-zoster virus gene product encoded by open reading frame 35 in viral replication in vitro and in differentiated human skin and T cells in vivo.Journal of virology · 2005Article
- Peculiarities of herpes simplex virus (HSV) transcription: an overview.Virus genes · 2004Review
- ICP27 selectively regulates the cytoplasmic localization of a subset of viral transcripts in herpes simplex virus type 1-infected cells.Journal of virology · 2004Article
- The human cytomegalovirus UL97 protein kinase, an antiviral drug target, is required at the stage of nuclear egress.Journal of virology · 2003Article
- Identification, localization, and regulation of expression of the UL24 protein of herpes simplex virus type 1.Journal of virology · 2002Article
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5 authors.
Funding
Abstract
Herpes simplex virus specifies two sets of transcripts from the UL24 gene, short transcripts (e.g., 1.4 kb), processed at the UL24 poly(A) site, and long transcripts (e.g., 5.6 kb), processed at the UL26 poly(A) site. The 1.4- and 5.6-kb transcripts initiate from the same promoter but are expressed with early and late kinetics, respectively. Measurements of transcript levels following actinomycin D treatment of infected cells revealed that the 1.4- and 5.6-kb UL24 transcripts have similar stabilities, consistent with UL24 transcript kinetics being regulated by differential polyadenylation rather than by differential stabilities. Although the UL24 poly(A) site, which gives rise to short transcripts, is encountered first during processing, long transcripts processed at the UL26 site are equally or more abundant; thus, operationally, the UL24 site is weak. Using a series of viral ICP27 mutants, we investigated whether ICP27, which has been suggested to stimulate the usage of weak poly(A) sites, stimulates 1.4-kb transcript accumulation. We found that accumulation of 1.4-kb transcripts did not require ICP27 during viral infection. Rather, ICP27 was required for full expression of 5.6-kb transcripts, and the decrease in 5. 6-kb transcripts relative to 1.4-kb transcripts was not due solely to reduced DNA synthesis. Our results indicate that temporal expression of UL24 transcripts can be regulated by differential polyadenylation and that although ICP27 is not required for processing at the operationally weak UL24 poly(A) site, it does modulate 5.6-kb transcript levels at a step subsequent to transcriptional initiation.
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