ArticlePloS one2013
Eight nucleotide substitutions inhibit splicing to HPV-16 3'-splice site SA3358 and reduce the efficiency by which HPV-16 increases the life span of primary human keratinocytes.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- The Involvement of LvSRSF2 in Circular RNA Biogenesis and Its Role in Immunity Against White Spot Syndrome Virus (WSSV) inInternational journal of molecular sciences · 2025Article
- The splicing factor kinase, SR protein kinase 1 (SRPK1) is essential for late events in the human papillomavirus life cycle.PLoS pathogens · 2025Article
- hnRNP H controls alternative splicing of human papillomavirus type 16 E1, E6, E7, and E6^E7 mRNAs via GGG motifs.Journal of virology · 2024Article
- Review
- A novel HPV16 splicing enhancer critical for viral oncogene expression and cell immortalization.Nucleic acids research · 2024Article
- Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024Review
- Towards understandings of serine/arginine-rich splicing factors.Acta pharmaceutica Sinica. B · 2023Review
- HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation.International journal of molecular sciences · 2022Review
- hnRNP G/RBMX enhances HPV16 E2 mRNA splicing through a novel splicing enhancer and inhibits production of spliced E7 oncogene mRNAs.Nucleic acids research · 2022Article
- Overexpression of m6A-factors METTL3, ALKBH5, and YTHDC1 alters HPV16 mRNA splicing.Virus genes · 2022Article
- HnRNP D activates production of HPV16 E1 and E6 mRNAs by promoting intron retention.Nucleic acids research · 2022Article
- Identification of heterogenous nuclear ribonucleoproteins (hnRNPs) and serine- and arginine-rich (SR) proteins that induce human papillomavirus type 16 late gene expression and alter L1 mRNA splicing.Archives of virology · 2022Article
- Extrachromosomal DNA in HPV-Mediated Oropharyngeal Cancer Drives Diverse Oncogene Transcription.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Review
- Heterogeneous Nuclear Ribonucleoprotein A1 (hnRNP A1) and hnRNP A2 Inhibit Splicing to Human Papillomavirus 16 Splice Site SA409 through a UAG-Containing Sequence in the E7 Coding Region.Journal of virology · 2020Article
- 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
- The DNA damage response activates HPV16 late gene expression at the level of RNA processing.Nucleic acids research · 2018Article
- Review
- hnRNP L controls HPV16 RNA polyadenylation and splicing in an Akt kinase-dependent manner.Nucleic acids research · 2017Article
Corrections and comments
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The most commonly used 3'-splice site on the human papillomavirus type 16 (HPV-16) genome named SA3358 is used to produce HPV-16 early mRNAs encoding E4, E5, E6 and E7, and late mRNAs encoding L1 and L2. We have previously shown that SA3358 is suboptimal and is totally dependent on a downstream splicing enhancer containingmultiple potential ASF/SF2 binding sites. Here weshow that only one of the predicted ASF/SF2 sites accounts for the majority of the enhancer activity. We demonstrate that single nucleotide substitutions in this predicted ASF/SF2 site impair enhancer function and that this correlates with less efficient binding to ASF/SF2 in vitro. We provide evidence that HPV-16 mRNAs that arespliced to SA3358 interact with ASF/SF2 in living cells. In addition,mutational inactivation of the ASF/SF2 site weakened the enhancer at SA3358 in episomal forms of the HPV-16 genome, indicating that the enhancer is active in the context of the full HPV-16 genome.This resulted in induction of HPV-16 late gene expression as a result of competition from late splice site SA5639. Furthermore, inactivation of the ASF/SF2 site of the SA3358 splicing enhancer reduced the ability of E6- and E7-encoding HPV-16 plasmids to increase the life span of primary keratinocytes in vitro, demonstrating arequirement for an intact splicing enhancer of SA3358 forefficient production of the E6 and E7 mRNAs. These results link the strength of the HPV-16 SA3358 splicing enhancer to expression of E6 and E7 and to the pathogenic properties of HPV-16.
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