ArticleJournal of virology2005
A 57-nucleotide upstream early polyadenylation element in human papillomavirus type 16 interacts with hFip1, CstF-64, hnRNP C1/C2, and polypyrimidine tract binding protein.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- The host geneActa biochimica et biophysica Sinica · 2024Article
- Review
- Cells with stem-like properties are associated with the development of HPV18-positive cervical cancer.Cancer science · 2023Article
- HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation.International journal of molecular sciences · 2022Review
- Review
- Stress proteins: the biological functions in virus infection, present and challenges for target-based antiviral drug development.Signal transduction and targeted therapy · 2020Review
- The Role of RNA Splicing Factors in Cancer: Regulation of Viral and Human Gene Expression in Human Papillomavirus-Related Cervical Cancer.Frontiers in cell and developmental biology · 2020Review
- Role of the DNA Damage Response in Human Papillomavirus RNA Splicing and Polyadenylation.International journal of molecular sciences · 2018Review
- hnRNP L controls HPV16 RNA polyadenylation and splicing in an Akt kinase-dependent manner.Nucleic acids research · 2017Article
- Review
- Control of human papillomavirus gene expression by alternative splicing.Virus research · 2017Review
- Splicing and Polyadenylation of Human Papillomavirus Type 16 mRNAs.International journal of molecular sciences · 2017Review
- Serine/Arginine-Rich Splicing Factor 3 and Heterogeneous Nuclear Ribonucleoprotein A1 Regulate Alternative RNA Splicing and Gene Expression of Human Papillomavirus 18 through Two Functionally Distinguishable cis Elements.Journal of virology · 2016Article
- A comprehensive analysis of 3' end sequencing data sets reveals novel polyadenylation signals and the repressive role of heterogeneous ribonucleoprotein C on cleavage and polyadenylation.Genome research · 2016Article
- Heterogeneous Nuclear Ribonucleoprotein C Proteins Interact with the Human Papillomavirus Type 16 (HPV16) Early 3'-Untranslated Region and Alleviate Suppression of HPV16 Late L1 mRNA Splicing.The Journal of biological chemistry · 2015Article
- RNA Binding Proteins that Control Human Papillomavirus Gene Expression.Biomolecules · 2015Review
- Arginine methylation and citrullination of splicing factor proline- and glutamine-rich (SFPQ/PSF) regulates its association with mRNA.RNA (New York, N.Y.) · 2015Article
- Suppression of HPV-16 late L1 5'-splice site SD3632 by binding of hnRNP D proteins and hnRNP A2/B1 to upstream AUAGUA RNA motifs.Nucleic acids research · 2013Article
- Regulation of human papillomavirus gene expression by splicing and polyadenylation.Nature reviews. Microbiology · 2013Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the role of the human papillomavirus type 16 (HPV-16) early untranslated region (3' UTR) in HPV-16 gene expression. We found that deletion of the early 3' UTR reduced the utilization of the early polyadenylation signal and, as a consequence, resulted in read-through into the late region and production of late L1 and L2 mRNAs. Deletion of the U-rich 3' half of the early 3' UTR had a similar effect, demonstrating that the 57-nucleotide U-rich region acted as an enhancing upstream element on the early polyadenylation signal. In accordance with this, the newly identified hFip1 protein, which has been shown to enhance polyadenylation through U-rich upstream elements, interacted specifically with the HPV-16 upstream element. This upstream element also interacted specifically with CstF-64, hnRNP C1/C2, and polypyrimidine tract binding protein, suggesting that these factors were either enhancing or regulating polyadenylation at the HPV-16 early polyadenylation signal. Mutational inactivation of the early polyadenylation signal also resulted in increased late mRNA production. However, the effect was reduced by the activation of upstream cryptic polyadenylation signals, demonstrating the presence of additional strong RNA elements downstream of the early polyadenylation signal that direct cleavage and polyadenylation to this region of the HPV-16 genome. In addition, we identified a 3' splice site at genomic position 742 in the early region with the potential to produce E1 and E4 mRNAs on which the E1 and E4 open reading frames are preceded only by the suboptimal E6 AUG. These mRNAs would therefore be more efficiently translated into E1 and E4 than previously described HPV-16 E1 and E4 mRNAs on which E1 and E4 are preceded by both E6 and E7 AUGs.
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