p53-mediated repression of nuclear factor-κB RelA via the transcriptional integrator p300

Rajani Ravi, Bijoyesh Mookerjee, Yvette Van Hensbergen, Gauri C. Bedi, Antonio Giordano, Wafik S. El-Deiry, Ephraim J. Fuchs, Atul Bedi

Research output: Contribution to journalArticlepeer-review

140 Scopus citations


The p53 tumor suppressor gene plays an instrumental role in transcriptional regulation of target genes involved in cellular stress responses. p53-dependent transactivation and transrepression require its interaction with p300/CBP, a coactivator that also interacts with the ReIA subunit of nuclear factor-κB. We find that p53 inhibits RelA-dependent transactivation without altering ReIA expression or inducible κB-DNA binding. p53-mediated repression of RelA is relieved by p300 overexpression and the increased RelA activity conferred by p53-deficiency is counteracted by either transactivation domain-deficient p300 fragments that bind RelA or a transdominant mutant of IκBα. Our results suggest that p53 can regulate diverse κB-dependent cellular responses.

Original languageEnglish (US)
Pages (from-to)4531-4536
Number of pages6
JournalCancer Research
Issue number20
StatePublished - Oct 15 1998

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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