ArticleJournal of virology2004
Cell cycle arrest in G2 induces human immunodeficiency virus type 1 transcriptional activation through histone acetylation and recruitment of CBP, NF-kappaB, and c-Jun to the long terminal repeat promoter.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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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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
34 citing papers in PubMed, 50 citations in OpenAlex.
- The human chromatin remodeling complex p400 restricts HIV-1 transcription in a Tat-dependent manner.Nucleic acids research · 2025Article
- Aminobisphosphonates reactivate the latent reservoir in people living with HIV-1.bioRxiv : the preprint server for biology · 2023Article
- Aminobisphosphonates reactivate the latent reservoir in people living with HIV-1.Frontiers in immunology · 2023Article
- The double-stranded RNA-binding protein, Staufen1, is an IRES-transacting factor regulating HIV-1 cap-independent translation initiation.Nucleic acids research · 2022Article
- Toxoplasma gondii ROP16 kinase silences the cyclin B1 gene promoter by hijacking host cell UHRF1-dependent epigenetic pathways.Cellular and molecular life sciences : CMLS · 2020Article
- Novel pathways of HIV latency reactivation revealed by integrated analysis of transcriptome and target profile of bryostatin.Scientific reports · 2020Article
- Dual Functionality of HIV-1 Vif in APOBEC3 Counteraction and Cell Cycle Arrest.Frontiers in microbiology · 2020Review
- Tat inhibition by didehydro-Cortistatin A promotes heterochromatin formation at the HIV-1 long terminal repeat.Epigenetics & chromatin · 2019Article
- Spontaneous reactivation of latent HIV-1 promoters is linked to the cell cycle as revealed by a genetic-insulators-containing dual-fluorescence HIV-1-based vector.Scientific reports · 2018Article
- Article
- Opposite transcriptional regulation of integrated vs unintegrated HIV genomes by the NF-κB pathway.Scientific reports · 2016Article
- Impact of Chromatin on HIV Replication.Genes · 2015Review
- Integrase inhibitor reversal dynamics indicate unintegrated HIV-1 dna initiate de novo integration.Retrovirology · 2015Article
- Manipulation of the host protein acetylation network by human immunodeficiency virus type 1.Critical reviews in biochemistry and molecular biology · 2015Review
- Translation initiation of the HIV-1 mRNA.Translation (Austin, Tex.) · 2014Review
- HIV-1 transcripts use IRES-initiation under conditions where Cap-dependent translation is restricted by poliovirus 2A protease.PloS one · 2014Article
- HIV-1 Vpr-a still "enigmatic multitasker".Frontiers in microbiology · 2014Review
- Impact of the Ku complex on HIV-1 expression and latency.PloS one · 2013Article
- Assessment of network perturbation amplitudes by applying high-throughput data to causal biological networks.BMC systems biology · 2012Article
- Regulation of Mycobacterium tuberculosis-dependent HIV-1 transcription reveals a new role for NFAT5 in the toll-like receptor pathway.PLoS pathogens · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In human immunodeficiency virus type 1 (HIV-1)-infected cells, a cell cycle arrest in G(2) increases viral expression and may represent a strategy for the virus to optimize its expression. In latently infected cells, balance between viral silencing and reactivation relies on the nucleosomal organization of the integrated long terminal repeat (LTR). It is shown here that nucleosome nuc-1, which is located downstream of the TATA box, is specifically modified when latently infected cells are arrested in G(2) by chemical inducers. Notably, histones H3 and H4 are hyperacetylated, and this modification is associated with an increased LTR-driven transcription. nuc-1 hyperacetylation is also associated with the recruitment of histone acetyltransferase CBP and transcription factors NF-kappaB and c-Jun. NF-kappaB and/or c-Jun binding to the LTR in G(2)-arrested cells appears to be required for CBP recruitment as well as for nuc-1 remodeling and viral reactivation.
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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.