c-Myc trans-activates the p53 promoter through a required downstream CACGTG motif.

D. Reisman, N. B. Elkind, B. Roy, J. Beamon, V. Rotter

Research output: Contribution to journalArticle

166 Citations (Scopus)

Abstract

c-Myc and wild-type p53 have been shown to play important roles in the regulation of cellular proliferation and oncogenic transformation. We have previously shown that the p53 promoter contains a conserved consensus recognition sequence for the basic-helix-loop-helix-containing proteins, identical to the specific binding site for c-Myc/Max heterodimers. Here, we demonstrate that this element, which is required for full promoter activity, is bound by in vitro translated c-Myc/Max heterodimers. Furthermore, we found that in cotransfection assays, c-Myc trans-activates the p53 promoter as well as a hybrid herpes simplex virus-thymidine kinase promoter containing multiple copies of a synthetic p53-derived c-Myc binding site. The p53 promoter deleted of the basic-helix-loop-helix consensus recognition sequence is not trans-activated by c-Myc, thus suggesting that c-Myc trans-activates the p53 promoter through the basic-helix-loop-helix recognition motif. These findings raise the possibility that the p53 gene may be a potential target for trans-activation by c-Myc in vivo.

Original languageEnglish
Pages (from-to)57-65
Number of pages9
JournalCell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
Volume4
Issue number2
Publication statusPublished - Feb 1993

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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