Differential phosphorylation of the signal-responsive domain of I kappa B alpha and I kappa B beta by I kappa B kinases

J Biol Chem. 2003 Aug 22;278(34):31980-7. doi: 10.1074/jbc.M304278200. Epub 2003 Jun 5.

Abstract

NF-kappa B activity is regulated by its association with the inhibitory I kappa B proteins, among which I kappa B alpha and I kappa B beta are the most abundant. I kappa B proteins are widely expressed in different cells and tissues and bind to similar combinations of NF-kappa B proteins. The degradation of I kappa B proteins allows nuclear translocation of NF-kappa B and hence plays a critical role in NF-kappa B activation. Previous studies have demonstrated that, although both I kappa B proteins are phosphorylated by the same I kappa B kinase (IKK) complex, and their ubiquitination and degradation following phosphorylation are carried out by the same ubiquitination/degradation machinery, their kinetics of degradation are quite different. To better understand the underlying mechanism of the differences in degradation kinetics, we have carried out a systematic, comparative analysis of the ability of the IKK catalytic subunits to phosphorylate I kappa B alpha and I kappa B beta. We found that, whereas IKK alpha is a weak kinase for the N-terminal serines of both I kappa B isoforms, IKK beta is an efficient kinase for those residues in I kappa B alpha. However, IKK beta phosphorylates the N-terminal serines of I kappa B beta far less efficiently, thereby providing an explanation for the slower rate of degradation observed for I kappa B beta. Mutational analysis indicated that the regions around the two N-terminal serines collectively influence the relative phosphorylation efficiency, and no individual residue is critical. These findings provide the first systematic analysis of the ability of I kappa B alpha and I kappa B beta to serve as substrates for IKKs and help provide a possible explanation for the differential degradation kinetics of I kappa B alpha and I kappa B beta.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Catalysis
  • Cell Line
  • Humans
  • I-kappa B Proteins / chemistry
  • I-kappa B Proteins / metabolism*
  • Kinetics
  • Mice
  • Mutagenesis, Site-Directed
  • Phosphorylation

Substances

  • I kappa B beta protein
  • I-kappa B Proteins