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Promoter scanning for transcription inhibition with DNA-binding polyamides

Academic Article
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Overview

authors

  • Ehley, J. A.
  • Melander, C.
  • Herman, D.
  • Baird, E. E.
  • Ferguson, H. A.
  • Goodrich, J. A.
  • Dervan, P. B.
  • Gottesfeld, Joel

publication date

  • March 2002

journal

  • Molecular and Cellular Biology  Journal

abstract

  • When targeted to sequences adjacent to a TATA element, pyrrole-imidazole (Py-Im) polyamides inhibit the DNA binding activity of TATA box binding protein (TBP) and basal transcription by RNA polymerase II. In the present study, we scanned the human immunodeficiency virus type 1 promoter for polyamide inhibition of TBP binding and transcription using a series of DNA constructs in which a polyamide binding site was placed at various distances from the TATA box. Polyamide interference with either TBP-DNA or TFIID-TFIIA-DNA contacts both upstream and downstream of the TATA element resulted in inhibition of transcription. Our results define important protein-DNA interactions outside of the TATA element and suggest that transcription inhibition of selected gene promoters can be achieved with polyamides that target unique sequences within these promoters at a distance from the TATA element. Our studies also demonstrate the utility of the Py-Im polyamides for discovery of functionally important protein-DNA contacts involved in transcription.

subject areas

  • Base Sequence
  • Binding Sites
  • Binding, Competitive
  • Cell-Free System
  • DNA Footprinting
  • DNA, Viral
  • DNA-Binding Proteins
  • HIV-1
  • Humans
  • Macromolecular Substances
  • Molecular Sequence Data
  • Mutagenesis, Site-Directed
  • Nylons
  • Promoter Regions, Genetic
  • Substrate Specificity
  • TATA Box
  • TATA-Box Binding Protein
  • Transcription Factor TFIIA
  • Transcription Factor TFIID
  • Transcription Factors
  • Transcription Factors, TFII
  • Transcription, Genetic
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Identity

International Standard Serial Number (ISSN)

  • 0270-7306

Digital Object Identifier (DOI)

  • 10.1128/mcb.22.6.1723-1733.2002

PubMed ID

  • 11865052
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Additional Document Info

start page

  • 1723

end page

  • 1733

volume

  • 22

issue

  • 6

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