MYBBP1a is a Novel Repressor of NF-κB

Heather R. Owen, Michael Elser, Edwin Cheung, Monika Gersbach, W. Lee Kraus, Michael O. Hottiger

Research output: Contribution to journalArticlepeer-review

57 Scopus citations


NF-κB is an inducible transcription factor activated in many different cell types by inflammatory and stress signals. The transcription of a wide variety of NF-κB genes is regulated by the coordinated action of transcription co-activators and co-repressors. Previously we identified Myb binding protein 1a (MYBBP1a) as an interaction partner of the transcription activation domain of RelA/p65. MYBBP1a has been shown by others to regulate various transcription factors, through largely unknown mechanisms. Here we present evidence that MYBBP1a is a novel co-repressor of NF-κB. MYBBP1a interacted directly with RelA/p65 and expression of MYBBP1a in cells repressed NF-κB dependent reporter expression but did affect neither RelA/p65 nuclear translocation nor its DNA binding activity. In vitro, MYBBP1a inhibited transcription from chromatinized templates at a step before pre-initiation complex formation. MYBBP1a was found to compete with the histone acetyl transferase co-activator, p300, for interaction with the transcription activation domain of RelA/p65. Expression levels of MYBBP1a are dependent on the cell type, and are particularly high in Jurkat T cells. These results indicate that MYBBP1a is a novel NF-κB co-repressor of transcription that competes with p300 and may function to regulate cell type specific genes.

Original languageEnglish (US)
Pages (from-to)725-736
Number of pages12
JournalJournal of Molecular Biology
Issue number3
StatePublished - Feb 23 2007


  • MYBBP1a
  • NF-kappa B
  • RelA
  • co-repressor
  • p65

ASJC Scopus subject areas

  • Structural Biology
  • Molecular Biology


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