ArticleNucleic acids research1995
Increasing binding of a transcription factor immediately downstream of the cap site of a cytomegalovirus gene represses expression.
Article in Nucleic acids research, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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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
7 citing papers in PubMed.
- Regulation of the MIE Locus During HCMV Latency and Reactivation.Pathogens (Basel, Switzerland) · 2020Review
- Molecular Determinants and the Regulation of Human Cytomegalovirus Latency and Reactivation.Viruses · 2018Review
- Human cytomegalovirus tropism for mucosal myeloid dendritic cells.Reviews in medical virology · 2014Review
- Layered PLG scaffolds for in vivo plasmid delivery.Biomaterials · 2009Article
- Effect of single-nucleotide polymorphisms of the 5' untranslated region of the human α-galactosidase gene on enzyme activity, and their frequencies in Portuguese caucasians.Journal of inherited metabolic disease · 2008Article
- The g.1170C>T polymorphism of the 5' untranslated region of the human alpha-galactosidase gene is associated with decreased enzyme expression--evidence from a family study.Journal of inherited metabolic disease · 2008Article
- Reactivation of the previously silenced cytomegalovirus major immediate-early promoter in the mouse liver: involvement of NFkappaB.Journal of virology · 1998Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
A closely related family of ubiquitous DNA binding proteins, called MDBP, binds with high affinity to two 14 base pair (bp) sites within the human cytomegalovirus immediate early gene 1 (CMV IE1) enhancer and with low affinity to one site beginning 5 bp downstream of the CMV IE1 transcription start point (+5 site). Unlike several cap position downstream MDBP sites in mammalian genes, these MDBP sites do not require cytosine methylation for optimal binding. Mutation of one of the enhancer MDBP sites to prevent MDBP recognition modestly increased the function of a neighboring CREB binding site in a transient transfection assay in the context of one promoter construct. A much larger effect on reporter gene expression (a 10-fold reduction) was seen when the low affinity MDBP recognition sequence at position +5 was converted to a high affinity site in a plasmid containing the CMV IE1 promoter upstream of the reporter gene. Evidence that the increased binding of MDBP at the mutant site is largely responsible for the observed results was provided by transfection experiments with this high affinity MDBP +5 site re-mutated to a non-binding site and by in vitro transcription assay.
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Registered trials
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