ArticleProceedings of the National Academy of Sciences of the United States of America2000
The human papillomavirus type 16 negative regulatory RNA element interacts with three proteins that act at different posttranscriptional levels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 58 citations in OpenAlex.
- Exploitation of host U2AF1 and U2AF2 splicing factors facilitates mosquito-borne orthoflavivirus infection across species.Nucleic acids research · 2026Article
- Playing both sides - Epstein-Barr Virus accumulates select cellular transcripts to counter virus-mediated host shut-off in lytic cells.PLoS pathogens · 2026Article
- Identifying regulatory elements and their RNA-binding proteins in the 3' untranslated regions of papillomavirus late mRNAs.Biomedical reports · 2024Article
- Review
- HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation.International journal of molecular sciences · 2022Review
- Strength in Diversity: Nuclear Export of Viral RNAs.Viruses · 2020Review
- Keratinocyte differentiation induces APOBEC3A, 3B, and mitochondrial DNA hypermutation.Scientific reports · 2018Article
- Review
- Splicing and Polyadenylation of Human Papillomavirus Type 16 mRNAs.International journal of molecular sciences · 2017Review
- HuR and Ago2 Bind the Internal Ribosome Entry Site of Enterovirus 71 and Promote Virus Translation and Replication.PloS one · 2015Article
- Productive Lifecycle of Human Papillomaviruses that Depends Upon Squamous Epithelial Differentiation.Frontiers in microbiology · 2012Article
- Construction of a full transcription map of human papillomavirus type 18 during productive viral infection.Journal of virology · 2011Article
- Human papillomavirus: gene expression, regulation and prospects for novel diagnostic methods and antiviral therapies.Future microbiology · 2010Review
- Sindbis virus usurps the cellular HuR protein to stabilize its transcripts and promote productive infections in mammalian and mosquito cells.Cell host & microbe · 2010Article
- The RNA stability regulator HuR regulates L1 protein expression in vivo in differentiating cervical epithelial cells.Virology · 2009Article
- Regulation of bovine papillomavirus type 1 gene expression by RNA processing.Frontiers in bioscience (Landmark edition) · 2009Review
- Human papillomavirus type 16 E2 protein transcriptionally activates the promoter of a key cellular splicing factor, SF2/ASF.Journal of virology · 2009Article
- HuR interacts with human immunodeficiency virus type 1 reverse transcriptase, and modulates reverse transcription in infected cells.Retrovirology · 2008Article
- Human papillomavirus type 16 late gene expression is regulated by cellular RNA processing factors in response to epithelial differentiation.Biochemical Society transactions · 2008Review
- The alternative splicing factor hnRNP A1 is up-regulated during virus-infected epithelial cell differentiation and binds the human papillomavirus type 16 late regulatory element.Virus research · 2008Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In human papillomaviruses, expression of the late genes L1 and L2, encoding the capsid proteins, is restricted to the upper layers of the infected epithelium. A 79-nt GU-rich negative regulatory element (NRE) located at the 3' untranslated region of the human papillomavirus 16 L1 gene was identified previously as key to the posttranscriptional control of late gene expression. Here, we demonstrate that in epithelial cells, the NRE can directly bind the U2 auxiliary splicing factor 65-kDa subunit, the cleavage stimulation factor 64-kDa subunit, and the Elav-like HuR protein. On induction of epithelial cell differentiation, levels of the U2 auxiliary splicing factor 65-kDa subunit decrease, levels of the cleavage stimulation factor 64-kDa subunit increase, and the levels of HuR remain unchanged, although redistribution of the HuR from the nucleus to the cytoplasm is observed. Late gene transcripts, which appear to be fully processed, are detected in undifferentiated W12 cells, but are confined in the nucleus. We propose that repression of late gene expression in basal epithelial cells may be caused by nuclear retention or cytoplasmic instability of NRE-containing late gene transcripts.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.