Degradation of promoter-bound p65/RelA is essential for the prompt termination of the nuclear factor kappaB response

J Exp Med. 2004 Jul 5;200(1):107-13. doi: 10.1084/jem.20040196. Epub 2004 Jun 28.

Abstract

Transcription factors of the nuclear factor (NF)-kappaB/Rel family translocate into the nucleus upon degradation of the IkappaBs. Postinduction repression of NF-kappaB activity depends on NF-kappaB-regulated resynthesis of IkappaBalpha, which dissociates NF-kappaB from DNA and exports it to the cytosol. We found that after activation, p65/RelA is degraded by the proteasome in the nucleus and in a DNA binding-dependent manner. If proteasome activity is blocked, NF-kappaB is not promptly removed from some target genes in spite of IkappaBalpha resynthesis and sustained transcription occurs. These results indicate that proteasomal degradation of p65/RelA does not merely regulate its stability and abundance, but also actively promotes transcriptional termination.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Active Transport, Cell Nucleus / physiology
  • Animals
  • Cysteine Endopeptidases / metabolism
  • Gene Expression Regulation*
  • Humans
  • I-kappa B Proteins / genetics
  • I-kappa B Proteins / metabolism
  • Mice
  • Multienzyme Complexes / metabolism
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / metabolism*
  • Promoter Regions, Genetic*
  • Proteasome Endopeptidase Complex
  • Protein Binding
  • Transcription Factor RelA
  • Transcription, Genetic
  • Ubiquitin / metabolism

Substances

  • I-kappa B Proteins
  • Multienzyme Complexes
  • NF-kappa B
  • NFKBIA protein, human
  • Nfkbia protein, mouse
  • Transcription Factor RelA
  • Ubiquitin
  • NF-KappaB Inhibitor alpha
  • Cysteine Endopeptidases
  • Proteasome Endopeptidase Complex