ArticleJournal of virology1998
Naturally occurring human immunodeficiency virus type 1 long terminal repeats have a frequently observed duplication that binds RBF-2 and represses transcription.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 42 citations in OpenAlex.
- A Canadian Survey of Research on HIV-1 Latency-Where Are We Now and Where Are We Heading?Viruses · 2024Review
- An additional NF-κB site allows HIV-1 subtype C to evade restriction by nuclear PYHIN proteins.Cell reports · 2021Article
- An emerging and variant viral promoter of HIV-1 subtype C exhibits low-level gene expression noise.Retrovirology · 2021Article
- The Evolution of Regulatory Elements in the Emerging Promoter-Variant Strains of HIV-1 Subtype C.Frontiers in microbiology · 2021Article
- Cat and Mouse: HIV Transcription in Latency, Immune Evasion and Cure/Remission Strategies.Viruses · 2019Review
- Distinctive variation in the U3R region of the 5' Long Terminal Repeat from diverse HIV-1 strains.PloS one · 2018Article
- ZASC1 stimulates HIV-1 transcription elongation by recruiting P-TEFb and TAT to the LTR promoter.PLoS pathogens · 2013Article
- Multiple NF-κB sites in HIV-1 subtype C long terminal repeat confer superior magnitude of transcription and thereby the enhanced viral predominance.The Journal of biological chemistry · 2012Article
- Identification and functional analysis of a second RBF-2 binding site within the HIV-1 promoter.Virology · 2011Article
- In search of a function for the most frequent naturally-occurring length polymorphism (MFNLP) of the HIV-1 LTR: retaining functional coupling, of Nef and RBF-2, at RBEIII?International journal of biological sciences · 2007Review
- Genetic analysis of the long terminal repeat (LTR) promoter region in HIV-1-infected individuals with different rates of disease progression.Virus genes · 2007Article
- MCEF is localized to the nucleus by protein sequences encoded within three distinct exons, where it represses HIV-1 Tat-transactivation of LTR-directed transcription.International journal of biological sciences · 2007Article
- Higher transactivation activity associated with LTR and Tat elements from HIV-1 BF intersubtype recombinant variants.Retrovirology · 2006Article
- Human immunodeficiency virus type 1 genetic diversity in the nervous system: evolutionary epiphenomenon or disease determinant?Journal of neurovirology · 2005Review
- TFII-I regulates induction of chromosomally integrated human immunodeficiency virus type 1 long terminal repeat in cooperation with USF.Journal of virology · 2005Article
- Human immunodeficiency virus type 1 subtypes have a distinct long terminal repeat that determines the replication rate in a host-cell-specific manner.Journal of virology · 2004Article
- In vitro activation of feline immunodeficiency virus in ramified microglial cells from asymptomatically infected cats.Journal of virology · 2001Article
- Functional differences between the long terminal repeat transcriptional promoters of human immunodeficiency virus type 1 subtypes A through G.Journal of virology · 2000Article
- A compilation of cellular transcription factor interactions with the HIV-1 LTR promoter.Nucleic acids research · 2000Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 38% of human immunodeficiency virus type 1 (HIV-1)-infected patients within the Vancouver Lymphadenopathy-AIDS Study have proviruses bearing partial 15- to 34-nucleotide duplications upstream of the NF-kappaB binding sites within the 5' long terminal repeat (LTR). This most frequent naturally occurring length polymorphism (MFNLP) of the HIV-1 5' LTR encompasses potential binding sites for several candidate transcription factors, including TCF-1alpha/hLEF, c-Ets, AP-4, and Ras-responsive binding factor 2 (RBF-2) (M. C. Estable et al., J. Virol. 70:4053-4062, 1996). RBF-2 and an apparently related factor, RBF-1, bind to at least four cis elements within the LTR which are required for full transcriptional responsiveness to protein-tyrosine kinases and v-Ras (B. Bell and I. Sadowski, Oncogene 13:2687-2697, 1996). Here we demonstrate that representative MFNLPs from two patients specifically bind RBF-2. In both cases, deletion of the MFNLP caused elevated LTR-directed transcription in cells expressing RBF-2 but not in cells with undetectable RBF-2. RBF-1, but not RBF-2, appears to contain the Ets transcription factor family member GABPalpha/GABPbeta1. Taken together with the fact that every MFNLP from a comparative study of over 500 LTR sequences from 42 patients contains a predicted binding site for RBF-2, our data suggest that the MFNLP is selected in vivo because it provides a duplicated RBF-2 cis element, which may limit transcription in monocytes and activated T cells.
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