ArticleJournal of virology2011
The cellular TAR RNA binding protein, TRBP, promotes HIV-1 replication primarily by inhibiting the activation of double-stranded RNA-dependent kinase PKR.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- TRBP modulates RLR signaling by inhibiting PKR-mediated antiviral stress granule formation.Scientific reports · 2025Article
- Review
- Double-stranded RNA induction asa potential dynamic biomarkerfor DNA-demethylating agents.Molecular therapy. Nucleic acids · 2022Article
- Arbovirus-vector protein interactomics identifies Loquacious as a co-factor for dengue virus replication in Aedes mosquitoes.PLoS pathogens · 2022Article
- The interaction between RPAP3 and TRBP reveals a possible involvement of the HSP90/R2TP chaperone complex in the regulation of miRNA activity.Nucleic acids research · 2022Article
- A tale of two proteins: PACT and PKR and their roles in inflammation.The FEBS journal · 2021Review
- Opposite actions of two dsRNA-binding proteins PACT and TRBP on RIG-I mediated signaling.The Biochemical journal · 2021Article
- Chicken-Derived Pattern Recognition Receptor chLGP2 Inhibits the Replication and Proliferation of Infectious Bronchitis Virus.Frontiers in microbiology · 2021Article
- Inhibition of PKR by Viruses.Frontiers in microbiology · 2021Review
- Shared Mechanisms Govern HIV Transcriptional Suppression in Circulating CD103Journal of virology · 2020Article
- Review
- Kinases: Understanding Their Role in HIV Infection.World journal of AIDS · 2019Article
- Crosstalk Between Mammalian Antiviral Pathways.Non-coding RNA · 2019Review
- Expression of TARBP1 protein in human non-small-cell lung cancer and its prognostic significance.Oncology letters · 2018Article
- ADAR1 and PACT contribute to efficient translation of transcripts containing HIV-1 trans-activating response (TAR) element.The Biochemical journal · 2017Article
- Mutant Cas9-transcriptional activator activates HIV-1 in U1 cells in the presence and absence of LTR-specific guide RNAs.Matters · 2017Article
- The TAR-RNA binding protein is required for immunoresponses triggered by Cardiovirus infection.Biochemical and biophysical research communications · 2016Article
- First Evidence for the Disease-Stage, Cell-Type, and Virus Specificity of microRNAs during Human Immunodeficiency Virus Type-1 Infection.Medical sciences (Basel, Switzerland) · 2016Article
- Movements of HIV-1 genomic RNA-APOBEC3F complexes and PKR reveal cytoplasmic and nuclear PKR defenses and HIV-1 evasion strategies.Virus research · 2016Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The TAR RNA binding protein, TRBP, is a cellular double-stranded RNA (dsRNA) binding protein that can promote the replication of HIV-1 through interactions with the viral TAR element as well as with cellular proteins that affect the efficiency of translation of viral transcripts. The structured TAR element, present on all viral transcripts, can impede efficient translation either by sterically blocking access of translation initiation factors to the 5'-cap or by activating the dsRNA-dependent kinase, PKR. Several mechanisms by which TRBP can facilitate translation of viral transcripts have been proposed, including the binding and unwinding of TAR and the suppression of PKR activation. Further, TRBP has been identified as a cofactor of Dicer in the processing of microRNAs (miRNAs), and sequestration of TRBP by TAR in infected cells has been proposed as a viral countermeasure to potential host cell RNA interference-based antiviral activities. Here, we have addressed the relative importance of these various roles for TRBP in HIV-1 replication. Using Jurkat T cells, primary human CD4(+) T cells, and additional cultured cell lines, we show that depletion of TRBP has no effect on viral replication when PKR activation is otherwise blocked. Moreover, the presence of TAR-containing mRNAs does not affect the efficacy of cellular miRNA silencing pathways. These results establish that TRBP, when expressed at physiological levels, promotes HIV-1 replication mainly by suppressing the PKR-mediated antiviral response, while its contribution to HIV-1 replication through PKR-independent pathways is minimal.
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