ArticleJournal of virology2007
Serine/arginine-rich proteins contribute to negative regulator of splicing element-stimulated polyadenylation in rous sarcoma virus.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- SRSF3 plays a key role in liver cancer sex disparity by facilitating hepatocyte expression of ERα and FOXA.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dysregulation of SRSF3/International journal of biological sciences · 2025Article
- The role of alternative pre-mRNA splicing in cancer progression.Cancer cell international · 2023Review
- Opposing roles of CLK SR kinases in controlling HIV-1 gene expression and latency.Retrovirology · 2022Article
- SRSF3 Expression Serves as a Potential Biomarker for Prognostic and Immune Response in Pan-Cancer.Frontiers in oncology · 2022Article
- Article
- SRSF3 and SRSF7 modulate 3'UTR length through suppression or activation of proximal polyadenylation sites and regulation of CFIm levels.Genome biology · 2021Article
- SRSF7 maintains its homeostasis through the expression of Split-ORFs and nuclear body assembly.Nature structural & molecular biology · 2020Article
- Emerging Roles of SRSF3 as a Therapeutic Target for Cancer.Frontiers in oncology · 2020Review
- Evidence that a threshold of serine/arginine-rich (SR) proteins recruits CFIm to promote rous sarcoma virus mRNA 3' end formation.Virology · 2016Article
- A genome landscape of SRSF3-regulated splicing events and gene expression in human osteosarcoma U2OS cells.Nucleic acids research · 2016Article
- Attenuation of the suppressive activity of cellular splicing factor SRSF3 by Kaposi sarcoma-associated herpesvirus ORF57 protein is required for RNA splicing.RNA (New York, N.Y.) · 2014Article
- Long-distance regulation of Add2 pre-mRNA3'end processing.RNA biology · 2013Article
- Juxtaposition of two distant, serine-arginine-rich protein-binding elements is required for optimal polyadenylation in Rous sarcoma virus.Journal of virology · 2011Article
- Nuclear pre-mRNA 3'-end processing regulates synapse and axon development in C. elegans.Development (Cambridge, England) · 2010Article
- Molecular mechanisms of eukaryotic pre-mRNA 3' end processing regulation.Nucleic acids research · 2010Review
- Polypyrimidine tract binding protein prevents activity of an intronic regulatory element that promotes usage of a composite 3'-terminal exon.The Journal of biological chemistry · 2009Article
- HIV-1 mRNA 3' end processing is distinctively regulated by eIF3f, CDK11, and splice factor 9G8.Molecular cell · 2009Article
- Inhibition of HIV-1 replication by eIF3f.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Functional interplay between viral and cellular SR proteins in control of post-transcriptional gene regulation.The FEBS journal · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Rous sarcoma virus (RSV) requires large amounts of unspliced RNA for replication. Splicing and polyadenylation are coupled in the cells they infect, which raises the question of how viral RNA is efficiently polyadenylated in the absence of splicing. Optimal RSV polyadenylation requires a far-upstream splicing control element, the negative regulator of splicing (NRS), that binds SR proteins and U1/U11 snRNPs and functions as a pseudo-5' splice site that interacts with and sequesters 3' splice sites. We investigated a link between NRS-mediated splicing inhibition and efficient polyadenylation. In vitro, the NRS alone activated a model RSV polyadenylation substrate, and while the effect did not require the snRNP-binding sites or a downstream 3' splice site, SR proteins were sufficient to stimulate polyadenylation. Consistent with this, SELEX-binding sites for the SR proteins ASF/SF2, 9G8, and SRp20 were able to stimulate polyadenylation when placed upstream of the RSV poly(A) site. In vivo, however, the SELEX sites improved polyadenylation in proviral clones only when the NRS-3' splice site complex could form. Deletions that positioned the SR protein-binding sites closer to the poly(A) site eliminated the requirement for the NRS-3' splice site interaction. This indicates a novel role for SR proteins in promoting RSV polyadenylation in the context of the NRS-3' splice site complex, which is thought to bridge the long distance between the NRS and poly(A) site. The results further suggest a more general role for SR proteins in polyadenylation of cellular mRNAs.
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Registered trials
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.