ArticleJournal of biomedicine & biotechnology2011
HDAC activity is required for efficient core promoter function at the mouse mammary tumor virus promoter.
Article in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Minireview: The versatile roles of lysine deacetylases in steroid receptor signaling.Molecular endocrinology (Baltimore, Md.) · 2014Review
- Visualizing epigenetics: current advances and advantages in HDAC PET imaging techniques.Neuroscience · 2014Review
- Class I lysine deacetylases facilitate glucocorticoid-induced transcription.The Journal of biological chemistry · 2013Article
- Roles of histone deacetylases in epigenetic regulation: emerging paradigms from studies with inhibitors.Clinical epigenetics · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylases (HDACs) have been shown to be required for basal or inducible transcription at a variety of genes by poorly understood mechanisms. We demonstrated previously that HDAC inhibition rapidly repressed transcription from the mouse mammary tumor virus (MMTV) promoter by a mechanism that does not require the binding of upstream transcription factors. In the current study, we find that HDACs work through the core promoter sequences of MMTV as well as those of several cellular genes to facilitate transcriptional initiation through deacetylation of nonhistone proteins.
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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.