Blog
About

12
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Mechanism of inhibition of RNA polymerase I transcription by DNA-dependent protein kinase.

      Biological chemistry

      Tumor Cells, Cultured, drug effects, Transcription, Genetic, biosynthesis, antagonists & inhibitors, RNA Polymerase I, pharmacology, Protein Kinases, Promoter Regions, Genetic, physiology, Pol1 Transcription Initiation Complex Proteins, Phosphorylation, Phosphoric Monoester Hydrolases, Humans, Enzyme Inhibitors, Electrophoretic Mobility Shift Assay, metabolism, DNA-Binding Proteins, DNA, Ribosomal, DNA Helicases, DNA, Blotting, Western, Antigens, Nuclear

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          DNA-dependent protein kinase represses RNA polymerase I (Pol I) transcription in vitro. To investigate the mechanism underlying transcriptional repression, we compared Pol I transcription in extracts from cells that either contain or lack the catalytic subunit of DNA-PK (DNA-PKcs). ATP-dependent repression of Pol I transcription was observed in extracts from DNA-PKcs-containing but not -deficient cells, required templates with free DNA ends, and was overcome by exogenous SL1, the factor that nucleates initiation complex formation. Order-of-addition experiments demonstrate that DNA-PKcs does not inactivate component(s) of the Poll transcription machinery. Instead, phosphorylated Ku protein competes with SL1 for binding to the rDNA promoter and, as a consequence, prevents initiation complex formation. The results reveal a novel mechanism of transcriptional regulation by DNA-PK. Once targeted to DNA, autophosphorylated Ku may displace positive- or negative-acting factors from their target sites, thereby repressing or activating transcription in a gene-specific manner.

          Related collections

          Author and article information

          Journal
          10.1515/BC.2002.189
          12530533

          Comments

          Comment on this article