ArticleJournal of virology1996
A fourth Sp1 site in the human immunodeficiency virus type 1 long terminal repeat is essential for negative-sense transcription.
Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- Article
- Origin and functional role of antisense transcription in endogenous and exogenous retroviruses.Retrovirology · 2023Review
- Retroviral Antisense Transcripts and Genes: 33 Years after First Predicted, a Silent Retroviral Revolution?Viruses · 2021Review
- Review
- Antisense Transcripts and Antisense Protein: A New Perspective on Human Immunodeficiency Virus Type 1.Frontiers in microbiology · 2020Review
- HIV-1 Antisense Protein of Different Clades Induces Autophagy and Associates with the Autophagy Factor p62.Journal of virology · 2019Article
- The sense behind retroviral anti-sense transcription.Virology journal · 2017Article
- Chromatin, non-coding RNAs, and the expression of HIV.Viruses · 2013Review
- HIV-1 antisense transcription is preferentially activated in primary monocyte-derived cells.Journal of virology · 2012Article
- Article
- HIV-1-encoded antisense RNA suppresses viral replication for a prolonged period.Retrovirology · 2012Article
- Complex role of microRNAs in HTLV-1 infections.Frontiers in genetics · 2012Article
- Human T-cell lymphotropic virus type 3 (HTLV-3)- and HTLV-4-derived antisense transcripts encode proteins with similar Tax-inhibiting functions but distinct subcellular localization.Journal of virology · 2011Article
- Antisense transcription in gammaretroviruses as a mechanism of insertional activation of host genes.Journal of virology · 2010Article
- Regulation of HIV-1 transcription in cells of the monocyte-macrophage lineage.Retrovirology · 2009Review
- Detection, characterization and regulation of antisense transcripts in HIV-1.Retrovirology · 2007Article
- HTLV-I antisense transcripts initiating in the 3'LTR are alternatively spliced and polyadenylated.Retrovirology · 2006Article
- A compilation of cellular transcription factor interactions with the HIV-1 LTR promoter.Nucleic acids research · 2000Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We report the discovery of a fourth Sp1 binding site at the 5' end of the U3 region of the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (HIV-1 Sp1 IV), localized to HXB2 nucleotides -433 to -441. This site is shown to bind Sp1 protein specifically in electrophoretic mobility shift assays. Sp1 protein appears to bind to HIV-1 Spl IV with 5 to 10 times lower affinity than to a consensus Sp1 site. Mutation of HIV-1 Sp1 IV in an HXB2-derived long terminal repeat-chloramphenicol acetyltransferase reporter construct gave no significant change in positive-sense transcription but abolished both basal and phorbol myristate acetate-activated negative-sense transcription. Taken together, the results further define the HIV-1 negative-sense promoter as an Sp1-dependent, phorbol myristate acetate-responsive, and Tat-inhibited promoter initiating at HXB2 nucleotide -450.
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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.