ArticleRNA (New York, N.Y.)2004
A novel function for Sam68: enhancement of HIV-1 RNA 3' end processing.
Article in RNA (New York, N.Y.), 2004. 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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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.
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- Cat and Mouse: HIV Transcription in Latency, Immune Evasion and Cure/Remission Strategies.Viruses · 2019Review
- Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections.Virology journal · 2015Article
- Placental Nkx2-5 and target gene expression in early-onset and severe preeclampsia.Hypertension in pregnancy · 2014Article
- Putting an 'End' to HIV mRNAs: capping and polyadenylation as potential therapeutic targets.AIDS research and therapy · 2013Article
- Thiouracil cross-linking mass spectrometry: a cell-based method to identify host factors involved in viral amplification.Journal of virology · 2013Article
- Thriving under stress: selective translation of HIV-1 structural protein mRNA during Vpr-mediated impairment of eIF4E translation activity.PLoS pathogens · 2012Article
- The Tpr protein regulates export of mRNAs with retained introns that traffic through the Nxf1 pathway.RNA (New York, N.Y.) · 2011Article
- Rev-free HIV-1 gene delivery system for targeting Rev-RRE-Crm1 nucleocytoplasmic RNA transport pathway.PloS one · 2011Article
- Molecular mechanisms of eukaryotic pre-mRNA 3' end processing regulation.Nucleic acids research · 2010Review
- Sam68 relocalization into stress granules in response to oxidative stress through complexing with TIA-1.Experimental cell research · 2009Article
- Human immunodeficiency virus type 1 (HIV-1) induces the cytoplasmic retention of heterogeneous nuclear ribonucleoprotein A1 by disrupting nuclear import: implications for HIV-1 gene expression.The Journal of biological chemistry · 2009Article
- Mechanisms employed by retroviruses to exploit host factors for translational control of a complicated proteome.Retrovirology · 2009Review
- Specific interaction between Sam68 and neuronal mRNAs: implication for the activity-dependent biosynthesis of elongation factor eEF1A.Journal of neuroscience research · 2009Article
- Selective translational repression of HIV-1 RNA by Sam68DeltaC occurs by altering PABP1 binding to unspliced viral RNA.Retrovirology · 2008Article
- Feline immunodeficiency virus OrfA alters gene expression of splicing factors and proteasome-ubiquitination proteins.Virology · 2008Article
- Gene regulatory networks in lactation: identification of global principles using bioinformatics.BMC systems biology · 2007Article
- hnRNP E1 and E2 have distinct roles in modulating HIV-1 gene expression.Retrovirology · 2007Article
- Use of modified U1 snRNAs to inhibit HIV-1 replication.Nucleic acids research · 2007Article
- The Wilms' tumor 1 (WT1) gene (+KTS isoform) functions with a CTE to enhance translation from an unspliced RNA with a retained intron.Genes & development · 2006Article
- The retrovirus RNA trafficking granule: from birth to maturity.Retrovirology · 2006Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both cis elements and host cell proteins can significantly affect HIV-1 RNA processing and viral gene expression. Previously, we determined that the exon splicing silencer (ESS3) within the terminal exon of HIV-1 not only reduces use of the adjacent 3' splice site but also prevents Rev-induced export of the unspliced viral RNA to the cytoplasm. In this report, we demonstrate that loss of unspliced viral RNA export is correlated with the inhibition of 3' end processing by the ESS3. Furthermore, we find that the host factor Sam68, a stimulator of HIV-1 protein expression, is able to reverse the block to viral RNA export mediated by the ESS3. The reversal is associated with a stimulation of 3' end processing of the unspliced viral RNA. Our findings identify a novel activity for the ESS3 and Sam68 in regulating HIV-1 RNA polyadenylation. Furthermore, the observations provide an explanation for how Sam68, an exclusively nuclear protein, modulates cytoplasmic utilization of the affected RNAs. Our finding that Sam68 is also able to enhance 3' end processing of a heterologous RNA raises the possibility that it may play a similar role in regulating host gene expression.
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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.