ArticleJournal of virology1997
Selection of a nonconsensus branch point is influenced by an RNA stem-loop structure and is important to confer stability to the herpes simplex virus 2-kilobase latency-associated transcript.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Human Cytomegalovirus RNA2.7 Is Required for Upregulating Multiple Cellular Genes To Promote Cell Motility and Viral Spread Late in Lytic Infection.Journal of virology · 2021Article
- Longitudinal transcriptomic characterization of viral genes in HSV-1 infected tree shrew trigeminal ganglia.Virology journal · 2020Article
- The effects of structure on pre-mRNA processing and stability.Methods (San Diego, Calif.) · 2017Review
- Viral noncoding RNAs: more surprises.Genes & development · 2015Review
- Stability determinants of murine cytomegalovirus long noncoding RNA7.2.Journal of virology · 2014Article
- A neuron-specific host microRNA targets herpes simplex virus-1 ICP0 expression and promotes latency.Cell host & microbe · 2014Article
- Article
- The half-life of the HSV-1 1.5-kb LAT intron is similar to the half-life of the 2.0-kb LAT intron.Journal of neurovirology · 2013Article
- Bovine Herpes Virus 1 (BHV-1) and Herpes Simplex Virus Type 1 (HSV-1) Promote Survival of Latently Infected Sensory Neurons, in Part by Inhibiting Apoptosis.Journal of cell death · 2013Review
- The molecular basis of herpes simplex virus latency.FEMS microbiology reviews · 2012Review
- Herpes simplex virus type 1 latency-associated transcript inhibits apoptosis and promotes neurite sprouting in neuroblastoma cells following serum starvation by maintaining protein kinase B (AKT) levels.The Journal of general virology · 2010Article
- Towards an understanding of the herpes simplex virus type 1 latency-reactivation cycle.Interdisciplinary perspectives on infectious diseases · 2010Article
- Two small RNAs encoded within the first 1.5 kilobases of the herpes simplex virus type 1 latency-associated transcript can inhibit productive infection and cooperate to inhibit apoptosis.Journal of virology · 2009Article
- Identification of two small RNAs within the first 1.5-kb of the herpes simplex virus type 1-encoded latency-associated transcript.Journal of neurovirology · 2008Article
- The stable 2-kilobase latency-associated transcript of herpes simplex virus type 1 can alter the assembly of the 60S ribosomal subunit and is exported from nucleus to cytoplasm by a CRM1-dependent pathway.Journal of virology · 2007Article
- Murine cytomegalovirus encodes a stable intron that facilitates persistent replication in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- The locus encompassing the latency-associated transcript of herpes simplex virus type 1 interferes with and delays interferon expression in productively infected neuroblastoma cells and trigeminal Ganglia of acutely infected mice.Journal of virology · 2005Article
- Human cytomegalovirus 5-kilobase immediate-early RNA is a stable intron.Journal of virology · 2004Article
- Construction of a herpes simplex virus type 1 mutant with only a three-nucleotide change in the branchpoint region of the latency-associated transcript (LAT) and the stability of its two-kilobase LAT intron.Journal of virology · 2004Article
- Mapping herpes simplex virus type 1 latency-associated transcript sequences that protect from apoptosis mediated by a plasmid expressing caspase-8.Journal of neurovirology · 2004Review
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3 authors.
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Abstract
Herpes simplex virus type 1 latent infection in sensory neurons is characterized by the highly restricted transcription of viral genes. The latency-associated transcripts (LAT) family members are the only transcripts that can be identified in large amounts in latently infected cells. The most abundant LAT species is a 2-kb RNA that results from splicing of a rare primary transcript. Analysis of a LAT mutant virus (TB1) in cell culture revealed an aberrant splicing pattern and production of a stable small (0.95-kb) LAT intron. A panel of deletion constructs expressing truncated LAT in transiently transfected cells mapped the region influencing stability to the 3' end of the LAT intron. This region encompasses the branch point and a putative stable stem-loop hairpin structure immediately upstream of the splice acceptor consensus polypyrimidine tract. Mutagenic analysis of the sequence in this region confirmed our hypothesis that the stem-loop structure is important for efficient splicing by influencing the selection of a nonconsensus branch point. Changes in this structure correlate with changes in branch point selection and production of an unstable 2-kb LAT.
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