ArticleMolecular and cellular biology1993
Transcription elongation in the human c-myc gene is governed by overall transcription initiation levels in Xenopus oocytes.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Transcriptional pause, arrest and termination sites for RNA polymerase II in mammalian N- and c-myc genes.Nucleic acids research · 1999Article
- Mitotic repression of RNA polymerase II transcription is accompanied by release of transcription elongation complexes.Molecular and cellular biology · 1997Article
- Repression of host RNA polymerase II transcription by herpes simplex virus type 1.Journal of virology · 1997Article
- Central nervous system-derived cells express a kappa B-binding activity that enhances human immunodeficiency virus type 1 transcription in vitro and facilitates TAR-independent transactivation by Tat.Journal of virology · 1994Article
- Premature termination of tubulin gene transcription in Xenopus oocytes is due to promoter-dependent disruption of elongation.Molecular and cellular biology · 1993Article
- Distinct properties of c-myc transcriptional elongation are revealed in Xenopus oocytes and mammalian cells and by template titration, 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), and promoter mutagenesis.Molecular and cellular biology · 1993Article
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2 authors at 1 institution in 1 country.
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Abstract
Both transcription initiation and transcription elongation contribute to the regulation of steady-state c-myc RNA levels. We have used the Xenopus oocyte transcription assay to study premature transcription termination which occurs in the first exon and intron of the human c-myc gene. Previous studies showed that after injection into Xenopus oocytes transcription from the c-myc P1 promoter resulted in read-through transcripts whereas transcription from the stronger P2 promoter resulted in a combination of prematurely terminated and read-through transcripts. We now demonstrate that this promoter-specific processivity results from the overall amount of RNA polymerase II transcription occurring from either promoter. Parameters that reduce the amount of transcription from P1 or P2, such as decreased concentration of template injected or decreased incubation time, result in a reduction in the ratio of terminated to read-through c-myc transcripts. Conversely, when transcription levels are increased by higher concentrations of injected template, increased incubation time, or coinjection with competing template, the ratio of terminated to read-through transcripts increases. We hypothesize that an RNA polymerase II processivity function is depleted above a threshold level of transcription initiation, resulting in high levels of premature transcription termination. These findings account for the promoter-specific effects on transcription elongation previously seen in this assay system and suggest a mechanism whereby limiting transcription elongation factors may contribute to transcription regulation in other eukaryotic cells.
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