ArticleNucleic acids research2022
HnRNP D activates production of HPV16 E1 and E6 mRNAs by promoting intron retention.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Cellular hnRNP D promotes influenza A virus replication by inhibiting TBK1-IRF3-mediated innate immune response.Journal of virology · 2026Article
- Molecular recognition and induced dimerization of hnRNP A2/B1 truncations by G-quadruplex single strand DNA.Scientific reports · 2026Article
- RNA splicing: Novel star in pulmonary diseases with a treatment perspective.Acta pharmaceutica Sinica. B · 2025Review
- 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
- HNRNPD regulates the biogenesis of circRNAs and the ratio of mRNAs to circRNAs for a set of genes.RNA biology · 2024Article
- Mature mRNA processing that deletes 3' end sequences directs translational activation and embryonic development.Science advances · 2023Article
- Role of Heterogeneous Nuclear Ribonucleoproteins in the Cancer-Immune Landscape.International journal of molecular sciences · 2023Review
- High-Risk Human Papillomavirus Oncogenic E6/E7 mRNAs Splicing Regulation.Frontiers in cellular and infection microbiology · 2022Review
- Editorial: The role of DNA viruses in human cancers.Frontiers in cellular and infection microbiology · 2022Article
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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
Human papillomavirus type 16 (HPV16) E1 and E6 proteins are produced from mRNAs with retained introns, but it has been unclear how these mRNAs are generated. Here, we report that hnRNP D act as a splicing inhibitor of HPV16 E1/E2- and E6/E7-mRNAs thereby generating intron-containing E1- and E6-mRNAs, respectively. N- and C-termini of hnRNP D contributed to HPV16 mRNA splicing control differently. HnRNP D interacted with the components of splicing machinery and with HPV16 RNA to exert its inhibitory function. As a result, the cytoplasmic levels of intron-retained HPV16 mRNAs were increased in the presence of hnRNP D. Association of hnRNP D with HPV16 mRNAs in the cytoplasm was observed, and this may correlate with unexpected inhibition of HPV16 E1- and E6-mRNA translation. Notably, hnRNP D40 interacted with HPV16 mRNAs in an HPV16-driven tonsillar cancer cell line and in HPV16-immortalized human keratinocytes. Furthermore, knockdown of hnRNP D in HPV16-driven cervical cancer cells enhanced production of the HPV16 E7 oncoprotein. Our results suggest that hnRNP D plays significant roles in the regulation of HPV gene expression and HPV-associated cancer development.
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