HDAC activity is required for efficient core promoter function at the mouse mammary tumor virus promoter.
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.
Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, 1703 E. Mabel Street, Tucson, AZ 85721-0207, USA.
Sang C
SC
Lee
Angeliki
A
Magklara
Catharine L
CL
Smith
D000818:Animals; D045744:Cell Line, Tumor; D006367:HeLa Cells; D056572:Histone Deacetylase Inhibitors / Q000494:pharmacology; D006655:Histone Deacetylases / Q000378:metabolism*; D006801:Humans; D006877:Hydroxamic Acids / Q000494:pharmacology; D008324:Mammary Tumor Virus, Mouse / Q000187:drug effects / Q000235:genetics*; D051379:Mice; D008957:Models, Genetic; D011401:Promoter Regions, Genetic; D012319:RNA Polymerase II / Q000378:metabolism; D016385:TATA Box / Q000235:genetics; D014158:Transcription, Genetic / Q000187:drug effects
D056572:Histone Deacetylase Inhibitors; D006877:Hydroxamic Acids; C012589:trichostatin A; D012319:RNA Polymerase II; D006655:Histone Deacetylases
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