p53 down-regulates human bradykinin B1 receptor gene expression

Francesca Bernassola, Maria Valeria Catani, Marco Corazzari, Antonello Rossi, Gerry Melino

Research output: Contribution to journalArticlepeer-review


The tumor suppressor, p53, has been shown to transcriptionally activate or silence a number of target genes. As an activator, p53 relies on its specific consensus sequence within the promoter. It is not clear whether p53 requires a specific DNA binding site in its action as a gene repressor. This report demonstrates that the human BKB1R gene is a p53 target. Expression of p53 in transiently transfected SV40-transformed IMR90 cells strongly suppressed luciferase reporter activity driven by a 1.8 kb BKB1R promoter as well as its minigene. These down-regulations were p53 dose-dependent, p53 reduced both basal and induced promoter activities of the minigene. Expression of p53 abolished the inducibility of the minigene. Induction of endogenous p53 expression by etoposide also inhibited promoter activity and minigene inducibility. Replacing the region containing both the putative p53 binding site and the TATA-box with a basal adenovirus promoter in the 1.8 kb promoter construct did not prevent p53 from inhibiting BKB1R promoter activity. Thus suppression by p53 is not mediated by competition with the TATA-binding protein and is not through interaction with the putative p53-binding site. p53 also does not appear to suppress BKB1R gene expression through interaction with c-Jun which functions in the inducibility of this gene [Yang et al., 2001].

Original languageEnglish
Pages (from-to)38-45
Number of pages8
JournalJournal of Cellular Biochemistry
Issue number1
Publication statusPublished - 2001


  • AP-1
  • Etoposide
  • Inducible expression
  • Minigene
  • p53 dominant negative
  • Tumor suppressor

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology


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