A crosstalk between hSiah2 and Pias E3-ligases modulates Pias-dependent activation

Oncogene. 2007 Oct 11;26(46):6665-76. doi: 10.1038/sj.onc.1210486. Epub 2007 May 28.

Abstract

Protein inhibitor of activated STAT (Pias) and human homologues of seven in absentia (hSiah) proteins both exhibit properties of ubiquitin-family peptides conjugating enzymes. Pias present E3-ligase activity for small ubiquitin-related modifiers (Sumo) covalent attachment to their targets. This post-translational modification is responsible for the activation of different transcription factors such as AP1. HSiah proteins possess ubiquitin-E3-ligase activity that triggers their partners to proteasomal-dependent degradation. The present study identifies Pias as a new hSiah2-interacting protein. We demonstrate that hSiah2 regulates specifically the proteasome-dependent degradation of Pias proteins. On reverse, Pias does not prevent hSiah2 degradation. We provide evidences for hSiah2-dependent degradation of Pias as being a mechanism in the regulation of c-jun N-terminal kinase-activating pathways. This report describes a new interconnection between sumoylation and ubiquitination pathways by regulating the levels of the E3-ligases available for these processes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Cell Nucleus / metabolism
  • Gene Expression Regulation
  • Humans
  • MAP Kinase Kinase 4 / metabolism
  • Nuclear Proteins / metabolism*
  • Proteasome Endopeptidase Complex / metabolism
  • Protein Inhibitors of Activated STAT / metabolism*
  • Proto-Oncogene Proteins c-jun / metabolism
  • SUMO-1 Protein / metabolism
  • Seven in Absentia Proteins
  • Transcriptional Activation
  • Ubiquitin-Protein Ligases / metabolism*
  • Ubiquitination

Substances

  • Nuclear Proteins
  • Protein Inhibitors of Activated STAT
  • Proto-Oncogene Proteins c-jun
  • SUMO-1 Protein
  • Ubiquitin-Protein Ligases
  • Seven in Absentia Proteins
  • MAP Kinase Kinase 4
  • Proteasome Endopeptidase Complex