Integrin-linked kinase regulates the nuclear entry of the c-Jun coactivator alpha-NAC and its coactivation potency

J Biol Chem. 2004 Oct 15;279(42):43893-9. doi: 10.1074/jbc.M406310200. Epub 2004 Aug 6.

Abstract

Overexpression of the integrin-linked kinase (ILK) was shown to increase c-Jun-dependent transcription. We now show that this effect of ILK involves the c-Jun transcriptional coactivator, nascent polypeptide-associated complex and coactivator alpha (alpha-NAC). ILK phosphorylated alpha-NAC on residue Ser-43 upon adhesion of cells to fibronectin. Co-expression of constitutively active ILK with alpha-NAC led to the nuclear accumulation of the coactivator. Conversely, alpha-NAC remained in the cytoplasm of cells transfected with a dominant-negative ILK mutant, and a mutated alpha-NAC at phosphoacceptor position Ser-43 (S43A) also localized outside of the nucleus. The S43A alpha-NAC mutant could not potentiate the effect of ILK on c-Jun-dependent transcription. We conclude that ILK-dependent phosphorylation of alpha-NAC induced the nuclear accumulation of the coactivator and that phosphorylation of alpha-NAC by ILK is required for the potentiation of c-Jun-mediated responses by the kinase. The results represent one of the rare examples of a transcriptional coactivator shuttling between the cytosol and the nucleus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • COS Cells
  • Cell Nucleus / enzymology*
  • Chlorocebus aethiops
  • DNA, Complementary / genetics
  • Kinetics
  • Molecular Chaperones
  • Phosphorylation
  • Phosphoserine / metabolism
  • Protein Serine-Threonine Kinases / metabolism*
  • Protein Transport / physiology
  • Proto-Oncogene Proteins c-jun / metabolism
  • Recombinant Proteins / metabolism
  • Trans-Activators / metabolism*
  • Transcription, Genetic
  • Transfection

Substances

  • DNA, Complementary
  • Molecular Chaperones
  • Proto-Oncogene Proteins c-jun
  • Recombinant Proteins
  • Trans-Activators
  • nascent-polypeptide-associated complex
  • Phosphoserine
  • integrin-linked kinase
  • Protein Serine-Threonine Kinases