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

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.

journal_name

Oncogene

journal_title

Oncogene

authors

Avantaggiati ML,Natoli G,Balsano C,Chirillo P,Artini M,De Marzio E,Collepardo D,Levrero M

subject

Has Abstract

pub_date

1993-06-01 00:00:00

pages

1567-74

issue

6

eissn

0950-9232

issn

1476-5594

journal_volume

8

pub_type

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