Transactivation by the hepatitis B virus X protein depends on AP-2 and other transcription factors

Nature. 1990 Mar 1;344(6261):72-4. doi: 10.1038/344072a0.

Abstract

The hepatitis B virus (HBV) X gene product (pX) could be important in disease pathogenesis because it is known to transactivate transcription from many viral and cellular gene promoters, including the HBV core gene promoter, the human immunodeficiency virus (HIV-1) long terminal repeat, and the c-myc promoter. We have previously shown that only a subset of the promoters that can be transactivated by pX is transactivated in any particular cell line, and have proposed that pX acts through multiple, cell type-specific transcription factors. We show here that pX acts through both AP-1 and AP-2 sites, and that pX has a transcription activation domain. We conclude that transactivation by pX depends on at least two distinct cellular DNA-binding transcription factors and we present a model for the action of pX.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cell Line
  • Chloramphenicol O-Acetyltransferase / genetics
  • DNA-Binding Proteins / physiology*
  • Enhancer Elements, Genetic / physiology
  • Humans
  • Molecular Sequence Data
  • Mutation
  • Plasmids
  • Recombinant Fusion Proteins / pharmacology
  • Simian virus 40 / genetics
  • Trans-Activators / physiology*
  • Transcription Factor AP-2
  • Transcription Factors / physiology*
  • Transcriptional Activation / physiology*

Substances

  • DNA-Binding Proteins
  • Recombinant Fusion Proteins
  • Trans-Activators
  • Transcription Factor AP-2
  • Transcription Factors
  • hepatitis B virus X protein
  • Chloramphenicol O-Acetyltransferase