ArticleJournal of molecular biology2011
HIV-1 replication and latency are regulated by translational control of cyclin T1.
Article in Journal of molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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
39 citing papers in PubMed, 58 citations in OpenAlex.
- Foxg1 and companions: Not only transcription factors.Neural regeneration research · 2026Article
- Review
- Structural rearrangements in the nucleus localize latent HIV proviruses to a perinucleolar compartment supportive of reactivation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- New insights into transcription elongation control of HIV-1 latency and rebound.Trends in immunology · 2023Review
- The Polyvalent Role of NF90 in RNA Biology.International journal of molecular sciences · 2022Review
- Heterogeneity of Latency Establishment in the Different Human CD4Journal of virology · 2022Article
- The Effect of miRNA Gene Regulation on HIV Disease.Frontiers in genetics · 2022Review
- Biogenesis of P-TEFb in CD4+ T cells to reverse HIV latency is mediated by protein kinase C (PKC)-independent signaling pathways.PLoS pathogens · 2021Article
- ILF3 Is a Negative Transcriptional Regulator of Innate Immune Responses and Myeloid Dendritic Cell Maturation.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- HSF1 inhibition attenuates HIV-1 latency reversal mediated by several candidate LRAs In Vitro and Ex Vivo.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Tat IRES modulator of tat mRNA (TIM-TAM): a conserved RNA structure that controls Tat expression and acts as a switch for HIV productive and latent infection.Nucleic acids research · 2020Article
- Latency-Reversing Agents Induce Differential Responses in Distinct Memory CD4 T Cell Subsets in Individuals on Antiretroviral Therapy.Cell reports · 2019Article
- Regulation of cyclin T1 during HIV replication and latency establishment in human memory CD4 T cells.Virology journal · 2019Article
- Serum deprivation/starvation leads to reactivation of HIV-1 in latently infected monocytes via activating ERK/JNK pathway.Scientific reports · 2018Article
- Nuclear factor 90 promotes angiogenesis by regulating HIF-1α/VEGF-A expression through the PI3K/Akt signaling pathway in human cervical cancer.Cell death & disease · 2018Article
- Promising Role of Toll-Like Receptor 8 Agonist in Concert with Prostratin for Activation of Silent HIV.Journal of virology · 2017Article
- Nuclear factor 90 uses an ADAR2-like binding mode to recognize specific bases in dsRNA.Nucleic acids research · 2016Article
- Article
- Cyclophilin B enhances HIV-1 infection.Virology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Human immunodeficiency virus (HIV) exploits cellular proteins during its replicative cycle and latent infection. The positive transcription elongation factor b (P-TEFb) is a key cellular transcription factor critical for these viral processes and is a drug target. During viral replication, P-TEFb is recruited via interactions of its cyclin T1 subunit with the HIV Tat (transactivator of transcription) protein and TAR (transactivation response) element. Through RNA silencing and over-expression experiments, we discovered that nuclear factor 90 (NF90), a cellular RNA binding protein, regulates P-TEFb expression. NF90 depletion reduced cyclin T1 protein levels by inhibiting translation initiation. Regulation was mediated by the 3' untranslated region of cyclin T1 mRNA independently of microRNAs. Cyclin T1 induction is involved in the escape of HIV-1 from latency. We show that the activation of viral replication by phorbol ester in latently infected monocytic cells requires the posttranscriptional induction of NF90 and cyclin T1, implicating NF90 in protein kinase C signaling pathways. This investigation reveals a novel mechanism of cyclin T1 regulation and establishes NF90 as a regulator of HIV-1 replication during both productive infection and induction from latency.
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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.