ArticleJournal of virology2013
Tra2-mediated recognition of HIV-1 5' splice site D3 as a key factor in the processing of vpr mRNA.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed.
- Review
- Review
- Transformer 2β regulates the alternative splicing of cell cycle regulatory genes to promote the malignant phenotype of ovarian cancer.Oncology research · 2023Article
- SRSF1 acts as an IFN-I-regulated cellular dependency factor decisively affecting HIV-1 post-integration steps.Frontiers in immunology · 2022Article
- Article
- SRSF10: an atypical splicing regulator with critical roles in stress response, organ development, and viral replication.RNA (New York, N.Y.) · 2021Review
- Increased Proviral DNA in Circulating Cells Correlates with Plasma Viral Rebound in Simian Immunodeficiency Virus-Infected Rhesus Macaques after Antiretroviral Therapy Interruption.Journal of virology · 2021Article
- Review
- Profiling of cis- and trans-acting factors supporting noncanonical splice site activation.RNA biology · 2021Article
- In-Depth Bioinformatic Analyses ofFrontiers in microbiology · 2020Article
- Gymnotic Delivery of LNA Mixmers Targeting Viral SREs Induces HIV-1 mRNA Degradation.International journal of molecular sciences · 2019Article
- Expression Level of HIV-1 Vif Can Be Fluctuated by Natural Nucleotide Variations in theFrontiers in microbiology · 2019Article
- Ranking noncanonical 5' splice site usage by genome-wide RNA-seq analysis and splicing reporter assays.Genome research · 2018Article
- Global synonymous mutagenesis identifies cis-acting RNA elements that regulate HIV-1 splicing and replication.PLoS pathogens · 2018Article
- Analysis of Competing HIV-1 Splice Donor Sites Uncovers a Tight Cluster of Splicing Regulatory Elements within Exon 2/2b.Journal of virology · 2017Article
- Succession of splicing regulatory elements determines cryptic 5΄ss functionality.Nucleic acids research · 2017Article
- Modulation of the splicing regulatory function of SRSF10 by a novel compound that impairs HIV-1 replication.Nucleic acids research · 2017Article
- Identification of small molecule modulators of HIV-1 Tat and Rev protein accumulation.Retrovirology · 2017Article
- Natural Single-Nucleotide Variations in the HIV-1 Genomic SA1prox Region Can Alter Viral Replication Ability by Regulating Vif Expression Levels.Journal of virology · 2016Article
- Balanced splicing at the Tat-specific HIV-1 3'ss A3 is critical for HIV-1 replication.Retrovirology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small noncoding HIV-1 leader exon 3 is defined by its splice sites A2 and D3. While 3' splice site (3'ss) A2 needs to be activated for vpr mRNA formation, the location of the vpr start codon within downstream intron 3 requires silencing of splicing at 5'ss D3. Here we show that the inclusion of both HIV-1 exon 3 and vpr mRNA processing is promoted by an exonic splicing enhancer (ESE(vpr)) localized between exonic splicing silencer ESSV and 5'ss D3. The ESE(vpr) sequence was found to be bound by members of the Transformer 2 (Tra2) protein family. Coexpression of these proteins in provirus-transfected cells led to an increase in the levels of exon 3 inclusion, confirming that they act through ESE(vpr). Further analyses revealed that ESE(vpr) supports the binding of U1 snRNA at 5'ss D3, allowing bridging interactions across the upstream exon with 3'ss A2. In line with this, an increase or decrease in the complementarity of 5'ss D3 to the 5' end of U1 snRNA was accompanied by a higher or lower vpr expression level. Activation of 3'ss A2 through the proposed bridging interactions, however, was not dependent on the splicing competence of 5'ss D3 because rendering it splicing defective but still competent for efficient U1 snRNA binding maintained the enhancing function of D3. Therefore, we propose that splicing at 3'ss A2 occurs temporally between the binding of U1 snRNA and splicing at D3.
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.