ArticleJournal of virology2001
Inhibition of human immunodeficiency virus type 1 Rev function by a dominant-negative mutant of Sam68 through sequestration of unspliced RNA at perinuclear bundles.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed.
- Host microRNA-31-5p regulates KHDRBS3 expression and modulates viral gene expression during KSHV lytic reactivation.Cell reports · 2026Article
- Structural basis of RNA recognition and dimerization by the STAR proteins T-STAR and Sam68.Nature communications · 2016Article
- Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections.Virology journal · 2015Article
- Nuclear Protein Sam68 Interacts with the Enterovirus 71 Internal Ribosome Entry Site and Positively Regulates Viral Protein Translation.Journal of virology · 2015Article
- Pokeweed antiviral protein alters splicing of HIV-1 RNAs, resulting in reduced virus production.RNA (New York, N.Y.) · 2014Article
- Unperturbed posttranscriptional regulatory Rev protein function and HIV-1 replication in astrocytes.PloS one · 2014Article
- Role of Sam68 in post-transcriptional gene regulation.International journal of molecular sciences · 2013Review
- Detection of viral RNA by fluorescence in situ hybridization (FISH).Journal of visualized experiments : JoVE · 2012Article
- Translational regulation of HIV-1 replication by HIV-1 Rev cellular cofactors Sam68, eIF5A, hRIP, and DDX3.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Article
- Sam68 relocalization into stress granules in response to oxidative stress through complexing with TIA-1.Experimental cell research · 2009Article
- Inhibition of HIV-1 gene expression by Sam68 Delta C: multiple targets but a common mechanism?Retrovirology · 2009Article
- Mechanisms employed by retroviruses to exploit host factors for translational control of a complicated proteome.Retrovirology · 2009Review
- Suppression of HIV-1 Nef translation by Sam68 mutant-induced stress granules and nef mRNA sequestration.Molecular cell · 2009Article
- 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
- The RNA-binding protein Sam68 contributes to proliferation and survival of human prostate cancer cells.Oncogene · 2007Article
- hnRNP E1 and E2 have distinct roles in modulating HIV-1 gene expression.Retrovirology · 2007Article
- Protein methylation is required to maintain optimal HIV-1 infectivity.Retrovirology · 2006Article
- Nuclear Factor 90, a cellular dsRNA binding protein inhibits the HIV Rev-export function.Retrovirology · 2006Article
- The retrovirus RNA trafficking granule: from birth to maturity.Retrovirology · 2006Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus (HIV) type 1 encodes an essential protein, Rev, which functions to transport unspliced and singly spliced viral transcripts from the nucleus to the cytoplasm to allow expression of the viral structural proteins. It has previously been reported that Sam68 synergistically stimulates Rev activity (T. Reddy et al., Nat. Med. 5:635-642, 1999). Here we report that the Sam68-like mammalian proteins SLM1 and SLM2 also stimulate Rev activity. Their stimulation ability cannot be attributed to a shuttling property, since Sam68, SLM1, and SLM2 do not display significant shuttling activity alone or in the presence of Rev. In addition, Sam68, SLM1, and SLM2 do not affect the equilibrium between unspliced and completely spliced HIV RNA. The C-terminally truncated Sam68 mutant (Sam68DeltaC) previously observed to inhibit the Sam68-mediated stimulation of Rev activity (Reddy et al., 1999) also inhibits SLM1- and SLM2-mediated stimulation of Rev activity. This suggests that the mechanism by which Sam68, SLM1, and SLM2 stimulate Rev activity may be common. Sam68DeltaC does not inhibit Rev activity by inhibiting Rev from shuttling between the nucleus and cytoplasm. Inhibition by Sam68DeltaC is a consequence of its mislocalization to the cytoplasm, as evidenced by the fact that addition of an exogenous nuclear localization signal to Sam68DeltaC restores nuclear localization and stimulation of Rev activity. We demonstrate that Sam68DeltaC causes perinuclear accumulation of unspliced HIV env RNA and propose that Sam68DeltaC inhibits Rev activity by sequestering Rev-responsive RNA away from the translation apparatus.
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