ArticleNucleic acids research2002
Efficient polyadenylation of Rous sarcoma virus RNA requires the negative regulator of splicing element.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- The gene-like promoter and transcription of LTR retrotransposons.bioRxiv : the preprint server for biology · 2026Article
- Stress proteins: the biological functions in virus infection, present and challenges for target-based antiviral drug development.Signal transduction and targeted therapy · 2020Review
- Evidence that a threshold of serine/arginine-rich (SR) proteins recruits CFIm to promote rous sarcoma virus mRNA 3' end formation.Virology · 2016Article
- 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
- Structural and functional analysis of the Rous Sarcoma virus negative regulator of splicing and demonstration of its activation by the 9G8 SR protein.Nucleic acids research · 2011Article
- Article
- RNA processing control in avian retroviruses.Frontiers in bioscience : a journal and virtual library · 2008Review
- Serine/arginine-rich proteins contribute to negative regulator of splicing element-stimulated polyadenylation in rous sarcoma virus.Journal of virology · 2007Article
- SR protein-mediated inhibition of CFTR exon 9 inclusion: molecular characterization of the intronic splicing silencer.Nucleic acids research · 2007Article
- The negative regulator of splicing element of Rous sarcoma virus promotes polyadenylation.Journal of virology · 2006Article
- The retrovirus RNA trafficking granule: from birth to maturity.Retrovirology · 2006Review
- A downstream polyadenylation element in human papillomavirus type 16 L2 encodes multiple GGG motifs and interacts with hnRNP H.Journal of virology · 2005Article
- Silent point mutation in an avian retrovirus RNA processing element promotes c-myb-associated short-latency lymphomas.Journal of virology · 2003Article
- Downstream elements of mammalian pre-mRNA polyadenylation signals: primary, secondary and higher-order structures.Nucleic acids research · 2003Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Rous sarcoma virus pre-mRNA contains an element known as the negative regulator of splicing (NRS) that acts to inhibit viral RNA splicing. The NRS binds serine/arginine-rich (SR) proteins, hnRNP H and the U1/U11 snRNPs, and appears to inhibit splicing by acting as a decoy 5' splice site. Deletions within the gag gene that encompass the NRS also lead to increased read-through past the viral polyadenylation site, suggesting a role for the NRS in promoting polyadenylation. Using NRS-specific deletions and mutations, we show here that a polyadenylation stimulatory activity maps directly to the NRS and is most likely dependent upon SR proteins and U1 and/or U11 snRNP. hnRNP H does not appear to mediate splicing control or stimulate RSV polyadenylation, since viral RNAs containing hnRNP H-specific mutations were spliced and polyadenylated normally. However, the ability of hnRNP H mutations to suppress the read-through caused by an SR protein mutation suggests the potential for hnRNP H to antagonize polyadenylation. Interestingly, disruption of splicing control closely correlated with increased read-through, indicating that a functional NRS is necessary for efficient RSV polyadenylation rather than binding of an individual factor. We propose a model in which the NRS serves to enhance polyadenylation of RSV unspliced RNA in a process analogous to the stimulation of cellular pre-mRNA polyadenylation by splicing complexes.
Indexed as
Identifiers
What OpenQuestion holds
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.