A palindromic element in the human immunodeficiency virus long terminal repeat binds retinoic acid receptors and can confer retinoic acid responsiveness on a heterologous promoter

J Acquir Immune Defic Syndr (1988). 1993 May;6(5):440-5.

Abstract

A palindromic element (site B) located between bases -328 and -347 (relative to the start site of transcription) of the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) was shown in a gel mobility shift assay to bind the human retinoic acid receptors (RARs). Greatly enhanced binding to this site was observed in the presence of both RAR and the retinoid X receptor. Retinoic acid responsiveness in F9 cells could be conferred on a thymidine kinase promoter by the presence of single or multiple copies of site B and responsiveness was abolished when this sequence was mutated to a form that could not bind RARs. However, the presence of this sequence did not render the HIV-1 LTR responsive to retinoic acid in F9 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Carrier Proteins / metabolism*
  • DNA-Binding Proteins / metabolism
  • Gene Expression Regulation, Viral*
  • HIV / genetics*
  • HIV Long Terminal Repeat / genetics*
  • HeLa Cells
  • Humans
  • In Vitro Techniques
  • Mice
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides / chemistry
  • Promoter Regions, Genetic*
  • Receptors, Cell Surface / metabolism
  • Receptors, Retinoic Acid
  • Retinoid X Receptors
  • Transcription Factors*
  • Tretinoin / pharmacology
  • Tumor Cells, Cultured

Substances

  • Carrier Proteins
  • DNA-Binding Proteins
  • Oligodeoxyribonucleotides
  • Receptors, Cell Surface
  • Receptors, Retinoic Acid
  • Retinoid X Receptors
  • Transcription Factors
  • Tretinoin