ArticleProceedings of the National Academy of Sciences of the United States of America1996
Activation domain-mediated enhancement of activator binding to chromatin in mammalian cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Relaxed repression of herpes simplex virus type 1 genomes in Murine trigeminal neurons.Journal of virology · 2007Article
- Single-molecule and population probing of chromatin structure using DNA methyltransferases.Methods (San Diego, Calif.) · 2007Article
- AtSAP18, an orthologue of human SAP18, is involved in the regulation of salt stress and mediates transcriptional repression in Arabidopsis.Plant molecular biology · 2006Article
- In vivo HP1 targeting causes large-scale chromatin condensation and enhanced histone lysine methylation.Molecular and cellular biology · 2005Article
- Enhancer sequences influence the role of the amino-terminal domain of bicoid in transcription.Molecular and cellular biology · 2003Article
- Regions of GAL4 critical for binding to a promoter in vivo revealed by a visual DNA-binding analysis.The EMBO journal · 2003Article
- GCN5 dependence of chromatin remodeling and transcriptional activation by the GAL4 and VP16 activation domains in budding yeast.Molecular and cellular biology · 2001Article
- Mechanisms of human papillomavirus E2-mediated repression of viral oncogene expression and cervical cancer cell growth inhibition.Journal of virology · 2000Article
- A general strategy to enhance the potency of chimeric transcriptional activators.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Chromatin opening and transactivator potentiation by RAP1 in Saccharomyces cerevisiae.Molecular and cellular biology · 1999Article
- Activation domain-specific and general transcription stimulation by native histone acetyltransferase complexes.Molecular and cellular biology · 1999Article
- SWI-SNF complex participation in transcriptional activation at a step subsequent to activator binding.Molecular and cellular biology · 1998Article
- Gal4p-mediated chromatin remodeling depends on binding site position in nucleosomes but does not require DNA replication.Molecular and cellular biology · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA binding by transcriptional activators is typically an obligatory step in the activation of gene expression. Activator binding and subsequent steps in transcription are repressed by genomic chromatin. Studies in vitro have suggested that overcoming this repression is an important function of some activation domains. Here we provide quantitative in vivo evidence that the activation domain of GAL4-VP16 can increase the affinity of GAL4 for its binding site on genomic DNA in mammalian cells. Moreover, the VP16 activation domain has a much greater stimulatory effect on expression from a genomic reporter gene than on a transiently transfected reporter gene, where factor binding is more permissive. We found that not all activation domains showed a greater activation potential in a genomic context, suggesting that only some activation domains can function in vivo to alleviate the repressive effects of chromatin. These data demonstrate the importance of activation domains in relieving chromatin-mediated repression in vivo and suggest that one way they function is to increase binding of the activator itself.
Indexed as
Identifiers
What OpenQuestion holds
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.