ArticleVirus genes2007
Induction of chromosomally integrated HIV-1 LTR requires RBF-2 (USF/TFII-I) and Ras/MAPK signaling.
Article in Virus genes, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 55 citations in OpenAlex.
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- A Canadian Survey of Research on HIV-1 Latency-Where Are We Now and Where Are We Heading?Viruses · 2024Review
- Ectopic USP15 expression inhibits HIV-1 transcription involving changes in YY1 deubiquitination and stability.Frontiers in cellular and infection microbiology · 2024Article
- A histone deacetylase network regulates epigenetic reprogramming and viral silencing in HIV-infected cells.Cell chemical biology · 2023Article
- Human lysyl-tRNA synthetase phosphorylation promotes HIV-1 proviral DNA transcription.Nucleic acids research · 2023Article
- CDK8 inhibitors antagonize HIV-1 reactivation and promote provirus latency in T cells.Journal of virology · 2023Article
- Upstream Stimulatory Factors Regulate HIV-1 Latency and Are Required for Robust T Cell Activation.Viruses · 2023Article
- TRIM5α recruits HDAC1 to p50 and Sp1 and promotes H3K9 deacetylation at the HIV-1 LTR.Nature communications · 2023Article
- TRIM24 controls induction of latent HIV-1 by stimulating transcriptional elongation.Communications biology · 2023Article
- Inhibition of the TRIM24 bromodomain reactivates latent HIV-1.Scientific reports · 2023Article
- Sense-and-Respond Payload Delivery Using a Novel Antigen-Inducible Promoter Improves Suboptimal CAR-T Activation.ACS synthetic biology · 2022Article
- Cryptosporidial Infection Suppresses Intestinal Epithelial Cell MAPK Signaling Impairing Host Anti-Parasitic Defense.Microorganisms · 2021Article
- Cellular Gene Modulation of HIV-Infected CD4 T Cells in Response to Serial Treatment with the Histone Deacetylase Inhibitor Vorinostat.Journal of virology · 2020Article
- Strategies to eradicate HIV from infected patients: elimination of latent provirus reservoirs.Cellular and molecular life sciences : CMLS · 2019Review
- Cat and Mouse: HIV Transcription in Latency, Immune Evasion and Cure/Remission Strategies.Viruses · 2019Review
- Real-time visualization of chromatin modification in isolated nuclei.Journal of cell science · 2017Article
- HIV-1 Latency and Eradication: Past, Present and Future.Current HIV research · 2016Review
- Impact of Chromatin on HIV Replication.Genes · 2015Review
- Post-transcriptional gene silencing, transcriptional gene silencing and human immunodeficiency virus.World journal of virology · 2015Review
- Epigenetic regulation of HIV-1 latency in astrocytes.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The HIV-1 LTR is regulated by multiple signaling pathways responsive to T cell activation. In this study, we have examined the contribution of the MAPK, calcineurin-NFAT and TNFalpha-NF-kappaB pathways on induction of chromosomally integrated HIV-1 LTR reporter genes. We find that induction by T-cell receptor (CD3) cross-linking and PMA is completely dependent upon a binding site for RBF-2 (USF1/2-TFII-I), known as RBEIII at -120. The MAPK pathway is essential for induction of the wild type LTR by these treatments, as the MEK inhibitors PD98059 and U0126 block induction by both PMA treatment and CD3 cross-linking. Stimulation of cells with ionomycin on its own has no effect on the integrated LTR, indicating that calcineurin-NFAT is incapable of causing induction in the absence of additional signals, but stimulation with both PMA and ionomycin produces a synergistic response. In contrast, stimulation of NF-kappaB by treatment with TNFalpha causes induction of both the wild type and RBEIII mutant LTRs, an effect that is independent of MAPK signaling. USF1, USF2 and TFII-I from unstimulated cells are capable of binding RBEIII in vitro, and furthermore can be observed on the LTR in vivo by chromatin imunoprecipitation from untreated cells. DNA binding activity of USF1/2 is marginally stimulated by PMA/ ionomycin treatment, and all three factors appear to remain associated with the LTR throughout the course of induction. These results implicate major roles for the MAPK pathway and RBF-2 (USF1/2-TFII-I) in coordinating events necessary for transition of latent integrated HIV-1 to active transcription in response to T cell signaling.
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