ArticleMolecular and cellular biology1994
A critical role for chromatin in mounting a synergistic transcriptional response to GAL4-VP16.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Gal4p-mediated chromatin remodeling depends on binding site position in nucleosomes but does not require DNA replication.Molecular and cellular biology · 1998Article
- Muscle LIM protein promotes myogenesis by enhancing the activity of MyoD.Molecular and cellular biology · 1997Article
- Three functional classes of transcriptional activation domain.Molecular and cellular biology · 1996Article
- Modulation of promoter occupancy by cooperative DNA binding and activation-domain function is a major determinant of transcriptional regulation by activators in vivo.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Activation domains of transcription factors mediate replication dependent transcription from a minimal HIV-1 promoter.Nucleic acids research · 1996Article
- GAL4-VP16 stimulates two RNA polymerase II promoters primarily at the preinitiation complex assembly step.Gene expression · 1996Article
- A single GAL4 dimer can maximally activate transcription under physiological conditions.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Binding of disparate transcriptional activators to nucleosomal DNA is inherently cooperative.Molecular and cellular biology · 1995Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The role of chromatin in mounting a synergistic transcriptional response to GAL4-VP16 was investigated. Strong synergy was observed when chromatin templates were used in vitro. The synergy was severely reduced when naked DNA templates were transcribed. In vivo synergy was strong when nonreplicating templates were used. However, the use of replicating templates, which involved transient disruptions of chromatin, led to strong reductions in synergy. In both of these low-synergy responses, transcription levels were high. We infer that strong synergy has a requirement for chromatin that may be understood in terms of the competition between multiple activator molecules and histone cores for promoter DNA.
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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.