Topic
Upstream activating sequence
About: Upstream activating sequence is a research topic. Over the lifetime, 1633 publications have been published within this topic receiving 100112 citations.
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TL;DR: The rat Ha-ras upstream sequence (-2876 to +986 bp relative to the most 5' transcriptional start site) was transcriptionally mapped at a gross level and analysed for autoregulation using co-transfection experiments to show that a fragment extending from - 2876 to -2110 bp contains a positive regulatory sequence.
Abstract: The rat Ha-ras upstream sequence (-2876 to +986 bp relative to the most 5' transcriptional start site) was transcriptionally mapped at a gross level. Ha-ras upstream sequence and 5' unidirectional deletion reporter constructs were transfected via particle bombardment into primary cultures of rat mammary epithelial cells. Analyses of Ha-ras reporter expression show that a fragment extending from -2876 to -2110 bp contains a positive regulatory sequence. The majority of Ha-ras expression is attributed to this sequence, since its deletion results in a 4-fold decrease in expression. The Ha-ras gene was also assessed for autoregulation using similar co-transfection experiments. Wild-type and activated (codon 12 G-->A transition) Ha-ras expression vectors, transcriptionally driven by Ha-ras upstream sequence, were co-transfected with Ha-ras upstream sequence deletion reporter constructs. The activated Ha-ras gene product induced its own transcription 2-fold, targeting the regulatory region between -2119 and -313 bp.
8 citations
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TL;DR: Net cis-acting promoter sequences for the mouse GPAT1 gene are identified: promoter 1a which includes part of the classical sequence and the downstream promoter 1b, indicating differential roles of the two promoters in the regulation of hepatic GPat1 gene expression in mice.
8 citations
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TL;DR: A strong promoter of bacteriophage MB78 does not have minus 35 consensus sequence although it has a TGn motif immediately upstream of minus 10 sequence as well as the AT rich UP element, and a phage-specific factor competes with sigma 70 RNA polymerase for binding to this region.
Abstract: A strong promoter of bacteriophage MB78 does not have minus 35 consensus sequence although it has a TGn motif immediately upstream of minus 10 sequence as well as the AT rich UP element. It is efficiently recognised by the sigma 70 RNA polymerase, however, a phage-specific factor competes with sigma 70 RNA polymerase for binding to this region, the binding of the factor being stronger than that of the polymerase. Contrary to the reports in the literature the polymerase appears not to bind to the UP element whereas the phage-specific factor does. The latter seems to be involved in the regulation of the promoter activity.
8 citations
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TL;DR: Both the promoter down phenotype of a mutation in UAS2 and increased activation when UAS1 was mutated reveal that the integrity of the U AS2 is required for the efficient activation of nifH promoter.
Abstract: The Azospirillum brasilense nifH promoter is positively controlled by the NifA protein bound to the upstream activator sequences (UASs). Two overlapping UASs located at −191 and −182 were identified with the consensus TGT-N10-ACA motif. The role of the two UASs of Azospirillum brasilense nifH promoter was examined by introducing base substitutions in the NifA binding sites. Both the promoter down phenotype of a mutation in UAS2 and increased activation when UAS1 was mutated reveal that the integrity of the UAS2 is required for the efficient activation of nifH promoter. This atypical NifA-binding site may represent a region interacting with two NifA dimers.Key words: Azospirillum brasilense, nif promoters, upstream activator sequence mutagenesis, NifA binding.
8 citations
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TL;DR: Evidence is presented for a new mechanism of Zap1‐mediated gene regulation and another way that this activator protein can repress protein expression in Saccharomyces cerevisiae.
Abstract: Maintaining zinc homeostasis is an important property of all organisms. In the yeast Saccharomyces cerevisiae, the Zap1 transcriptional activator is a central player in this process. In response to zinc deficiency, Zap1 activates transcription of many genes and consequently increases accumulation of their encoded proteins. In this report, we describe a new mechanism of Zap1-mediated regulation whereby increased transcription of certain target genes results in reduced protein expression. Transcription of the Zap1-responsive genes RTC4 and RAD27 increases markedly in zinc-deficient cells but, surprisingly, their protein levels decrease. We examined the underlying mechanism further for RTC4 and found that this unusual regulation results from altered transcription start site selection. In zinc-replete cells, RTC4 transcription begins near the protein-coding region and the resulting short transcript leader allows for efficient translation. In zinc-deficient cells, RTC4 RNA with longer transcript leaders are expressed that are not efficiently translated due to the presence of multiple small open reading frames upstream of the coding region. This regulation requires a potential Zap1 binding site located farther upstream of the promoter. Thus, we present evidence for a new mechanism of Zap1-mediated gene regulation and another way that this activator protein can repress protein expression.
8 citations