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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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Journal ArticleDOI
15 Jun 1999-Genomics
TL;DR: This study provides the first identification of the transcriptional control region of, and the basis for an understanding of the regulatory mechanism that controls, this kidney-specific, chloride-channel gene.

10 citations

Journal ArticleDOI
TL;DR: It is shown that the pyrrolizidine alkaloid heliotrine interferes with reporter signals derived from GAL4-based nuclear receptor transactivation assays by a mechanism independent of luciferase enzyme inhibition.

10 citations

Journal ArticleDOI
TL;DR: It is demonstrated here that the sequence lying about 700 bp upstream of the 5' end of the HSV-2 major LAT acts as a very strong promoter in transient expression assays in both neuronal and nonneuronal cells.
Abstract: In latently infected neurons, herpes simplex virus type 2 (HSV-2) expresses one abundant family of transcripts, the latency-associated transcripts (LATs). We demonstrate here that the sequence lying about 700 bp upstream of the 5' end of the HSV-2 major LAT acts as a very strong promoter in transient expression assays in both neuronal and nonneuronal cells. Transcription starts about 27 to 32 bp downstream of a functional TATA box. The proximal fragment from -102 to +34 includes the basal promoter and accounts for constitutive transcriptional activity in various cell lines. The distal region from -392 to -103 contributes to particularly strong promoter activity in neuronal cell lines and involves multiple cis-acting elements. A functional activating transcription factor/cyclic AMP (cAMP) response element binding protein motif lies just upstream of the TATA. By DNase I footprint and methylation protection assays, we identified several additional protein-binding sites upstream of the activating transcription factor/cAMP response element binding protein motif. A GC-rich element, termed LAT-3, was located between bases -128 to -102. A 2-bp substitution in LAT-3 markedly reduced promoter activity and abolished protein-binding ability in vitro. Gel retardation assay showed no competition for protein binding to LAT-3 by other GC-rich elements. LAT-3 appears to be a novel cis-acting element that may contribute to the neuronal responsiveness of the HSV-2 LAT promoter.

10 citations

Journal ArticleDOI
TL;DR: The 5S and 40S Ribo boxes are shown to be functionally interchangeable and to be conserved among the large rRNA genes of many organisms.
Abstract: In order to define the RNA polymerase I transcriptional apparatus and how it might interact with regulatory signals, the DNA sequences necessary for 40S rRNA transcription in Neurospora crassa were determined. A systematic set of deletion, substitution and insertion mutations were assayed in a homologous in vitro system. The sequences required for transcription of the gene consist of two large domains (I and II) from -113 to -37, and -29 to +4, respectively. Complete deletion of either domain abolished transcription. Upstream sequences confer a small stimulation of transcription. Domain II includes a TATA sequence at -5 which is sensitive to a small (2 bp) substitution and which is conserved among the large rRNA genes of many organisms. Domain I includes a sequence, termed the 'Ribo box', which is also required for transcription of the Neurospora 5S rRNA genes (1), and which occurs in the 5' region of a Neurospora ribosomal protein gene. The 5S and 40S Ribo boxes are shown to be functionally interchangeable.

10 citations

Journal ArticleDOI
TL;DR: The nucleotide sequence and in vivo transcription start sites for rrnA, one of the two r RNA gene clusters of the eubacterium Caulobacter crescentus, have been determined and there were two areas of homology when the major rRNA gene promoter was compared to the nucleotide sequences of the C. c Crescentus trpFBA promoter.

10 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20232
20223
20218
20206
20196
20186