ArticleMolecular cell2009
Suppression of HIV-1 Nef translation by Sam68 mutant-induced stress granules and nef mRNA sequestration.
Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- A novel SIV-infection animal model based on nude mice inoculated with MT-2 cells.Archives of virology · 2025Article
- Global profiling of arginine dimethylation in regulating protein phase separation by a steric effect-based chemical-enrichment method.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- The RNA binding protein Sam68 controls T helper 1 differentiation and anti-mycobacterial response through modulation of miR-29.Cell death and differentiation · 2019Article
- High expression of Sam68 in sacral chordomas is associated with worse clinical outcomes.OncoTargets and therapy · 2017Article
- Sam68 Is Required for DNA Damage Responses via Regulating Poly(ADP-ribosyl)ation.PLoS biology · 2016Article
- Sam68/KHDRBS1 is critical for colon tumorigenesis by regulating genotoxic stress-induced NF-κB activation.eLife · 2016Article
- Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections.Virology journal · 2015Article
- MDA5 localizes to stress granules, but this localization is not required for the induction of type I interferon.Journal of virology · 2013Article
- Inhibition of HIV-1 transcription and replication by a newly identified cyclin T1 splice variant.The Journal of biological chemistry · 2013Article
- Article
- Sam68 modulates the promoter specificity of NF-κB and mediates expression of CD25 in activated T cells.Nature communications · 2013Article
- HIV-1 Nef in macrophage-mediated disease pathogenesis.International reviews of immunology · 2012Review
- Herpes simplex virus 2 infection impacts stress granule accumulation.Journal of virology · 2012Article
- Diversity in genetic in vivo methods for protein-protein interaction studies: from the yeast two-hybrid system to the mammalian split-luciferase system.Microbiology and molecular biology reviews : MMBR · 2012Review
- Regulation of stress granules in virus systems.Trends in microbiology · 2012Review
- How do viruses interact with stress-associated RNA granules?PLoS pathogens · 2012Review
- Article
- Article
- 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
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
HIV-1 Nef plays important roles in HIV-1 replication and pathogenesis. It is translated from completely spliced HIV-1 RNA, and its expression is inherently regulated at the levels of viral DNA transcription and RNA splicing. Here we show that Sam68 cytoplasmic mutants potently suppress Nef expression. The suppression requires Sam68 domain aa 269-321 and is correlated with its ability to induce stress granules. In addition, the suppression is specific to Nef, and direct binding to nef mRNA 3'UTR confers the suppression specificity. Furthermore, nef mRNA is targeted to and enriched in these induced stress granules. Importantly, Nef suppression occurs in the context of HIV-1 infection of CD4+ T lymphocytes with little MHC I and CD4 downregulation. Taken together, these results demonstrate that stress granule induction and nef mRNA sequestration account for this translational suppression of Nef expression and offer a strategy for development of anti-HIV therapeutics to buttress our fight against HIV/AIDS.
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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.