The hepatitis B virus (HBV) pX transactivates the c-fos promoter through multiple cis-acting elements

Maria Laura Avantaggiati, Gioacchino Natoli, Clara Balsano, Paolo Chirillo, Marco Artini, Elisabetta De Marzio, Daniela Collepardo, Massimo Levrero

Research output: Contribution to journalArticlepeer-review

Abstract

The hepatitis B virus (HBV) X protein (pX) stimulates transcription regulated by cis-acting elements that control many viral and cellular genes, including the c-myc and the c-fos proto-oncogenes. Using several c-fos promoter deletion mutants, we found the serum-responsive element (SRE) located at - 315, the modified TPA-responsive element located at -296 (fos-AP-1 binding site, FAP) and the region spanning from nucleotide - 220 to - 120, which contains an NF1-like site and several stretches of sequence homologous to the AP-2 consensus binding sites, to be responsive to pX. pX does not modify the pattern of the retarded complexes bound to the SRE/FAP region which, in our system, appears to be occupied by SRE-binding factors. The activation of the SRE does not involve complex formation between SRE-binding factors and pX, it is not associated with an increase in serum response factor binding to the SRE and it does not determine changes in SRE mobility-shift pattern.

Original languageEnglish
Pages (from-to)1567-1574
Number of pages8
JournalOncogene
Volume8
Issue number6
Publication statusPublished - Jun 1993

ASJC Scopus subject areas

  • Cancer Research
  • Genetics
  • Molecular Biology

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