ArticleNucleic acids research1993
A nuclear protein with enhanced binding to methylated Sp1 sites in the AIDS virus promoter.
Article in Nucleic acids research, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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.
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- Balance between Retroviral Latency and Transcription: Based on HIV Model.Pathogens (Basel, Switzerland) · 2020Review
- 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
- Regulation of HIV-1 transcription in cells of the monocyte-macrophage lineage.Retrovirology · 2009Review
- Transcriptional suppression of in vitro-integrated human immunodeficiency virus type 1 does not correlate with proviral DNA methylation.Journal of virology · 2003Article
- 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 at 1 institution in 1 country.
Funding
Abstract
We report here the discovery of HMBP, a protein in nuclei of human T-helper lymphocytes and other human cell types, which binds with enhanced affinity to a promoter element in the HIV-1 long terminal repeat when that element is methylated at CpGs, the target site of the human DNA methyltransferase. This promoter element contains three (degenerate) binding sites for Sp1, a general activator of transcription. Gel shift assays and footprinting experiments indicate that HMBP binding overlaps two of these methylated Sp1 sites. Although HMBP binds these methylated Sp1 sites, it does not bind consensus Sp1 sites. Competition studies, differences in binding site specificities, binding conditions, and, in some cases, chromatographic separation further distinguish HMBP from Sp1 and from each of four previously identified methylated-DNA binding proteins. HMBP binds hemimethylated DNA in a strand dependent manner. These binding characteristics suggest that HMBP may recognize newly replicated DNA and thereby play a role in differentiation. If HMBP is able to compete with Sp1 for binding at methylated, non-consensus Sp1 sites in vivo and repress transcription, it may play a role in AIDS latency.
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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.