ArticleProceedings of the National Academy of Sciences of the United States of America1993
NF-IL6-mediated transcriptional activation of the long terminal repeat of the human immunodeficiency virus type 1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 105 citations in OpenAlex.
- Involvement of Human Cellular Proteins and Structures in Realization of the HIV Life Cycle: A Comprehensive Review, 2024.Viruses · 2024Review
- RPLP1 restricts HIV-1 transcription by disrupting C/EBPβ binding to the LTR.Nature communications · 2024Article
- Article
- Safe CRISPR-Cas9 Inhibition of HIV-1 with High Specificity and Broad-Spectrum Activity by Targeting LTR NF-κB Binding Sites.Molecular therapy. Nucleic acids · 2020Article
- Article
- Article
- Distinctive variation in the U3R region of the 5' Long Terminal Repeat from diverse HIV-1 strains.PloS one · 2018Article
- Functional Studies of CCAAT/Enhancer Binding Protein Site Located Downstream of the Transcriptional Start Site.Clinical medicine insights. Pathology · 2017Article
- Article
- Genotypic and phenotypic heterogeneity in the U3R region of HIV type 1 subtype C.AIDS research and human retroviruses · 2014Article
- Genetic variation and HIV-associated neurologic disease.Advances in virus research · 2013Review
- Mechanisms of HIV Transcriptional Regulation and Their Contribution to Latency.Molecular biology international · 2012Article
- Structural and functional studies of CCAAT/enhancer binding sites within the human immunodeficiency virus type 1 subtype C LTR.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2010Article
- Innate and adaptive factors regulating human immunodeficiency virus type 1 genomic activation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Review
- The macrophage in HIV-1 infection: from activation to deactivation?Retrovirology · 2010Review
- Host hindrance to HIV-1 replication in monocytes and macrophages.Retrovirology · 2010Review
- Regulation of SIV mac 239 basal long terminal repeat activity and viral replication in macrophages: functional roles of two CCAAT/enhancer-binding protein beta sites in activation and interferon beta-mediated suppression.The Journal of biological chemistry · 2010Article
- Regulation of HIV-1 transcription in cells of the monocyte-macrophage lineage.Retrovirology · 2009Review
- Oral infectious diseases: a potential risk factor for HIV virus recrudescence?Oral diseases · 2009Review
- CCAAT/enhancer-binding proteins and the pathogenesis of retrovirus infection.Future microbiology · 2009Review
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
An upstream control region in the long terminal repeat (LTR) of human immunodeficiency virus type 1 (HIV-1) includes a potential negative regulatory element (NRE1). Cotransfecting multimers of a sequence spanning this element with an LTR-CAT construct produced an increase in chloramphenicol acetyltransferase (CAT) activity in Jurkat and HepG2 cells, providing further evidence and support for the existence of an NRE. In screening experiments aimed at identifying those factors that regulate HIV-1 transcription through interactions with the NRE1 region, we isolated a cDNA for NF-IL6. Previous studies have shown that NF-IL6 is a key nuclear factor that activates gene expression in response to interleukin 6. By methylation interference analysis, we have localized the NF-IL6 binding site within the NRE1 region and found that it overlaps an E box that has previously been implicated as the binding element for a negative regulator of HIV-1 expression. Through a database search, we identified an additional consensus binding sequence for NF-IL6 in the LTR of many HIV-1 variants and found that over this sequence, purified NF-IL6 can produce an extended footprint that overlaps one of the binding sites for NF-kappa B. A product of the nf-il6 gene activated transcription from several LTR-CAT constructs in transient transfection assays. Thus, NF-IL6 could play a central role in the control of HIV-1 gene expression and this protein might be a key mediator in signaling pathways where HIV-1 is activated by interleukin 6.
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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.