The human COP9 signalosome protects ubiquitin-conjugating enzyme 3 (UBC3/Cdc34) from beta-transducin repeat-containing protein (betaTrCP)-mediated degradation. - Institut Pasteur Accéder directement au contenu
Article Dans Une Revue Journal of Biological Chemistry Année : 2010

The human COP9 signalosome protects ubiquitin-conjugating enzyme 3 (UBC3/Cdc34) from beta-transducin repeat-containing protein (betaTrCP)-mediated degradation.

Emmanuel Sechet
Florence Margottin-Goguet
Lars Rogge
  • Fonction : Auteur
Elisabetta Bianchi

Résumé

The COP9 signalosome (CSN) is an essential multisubunit complex that regulates the activity of cullin-RING ubiquitin ligases by removing the ubiquitin-like peptide NEDD8 from cullins. Here, we demonstrate that the CSN can affect other components of the ubiquitination cascade. Down-regulation of human CSN4 or CSN5 induced proteasome-mediated degradation of the ubiquitin-conjugating enzyme UBC3/Cdc34. UBC3 was targeted for ubiquitination by the cullin-RING ubiquitin ligase SCF(betaTrCP). This interaction required the acidic C-terminal extension of UBC3, which is absent in ubiquitin-conjugating enzymes of the UBCH5 family. Conversely, the UBC3 acidic domain was sufficient to impart sensitivity to SCF(betaTrCP)-mediated ubiquitination to UBCH5 enzymes. Our work indicates that the CSN is necessary to ensure the stability of selected ubiquitin-conjugating enzymes and uncovers a novel pathway of regulation of ubiquitination processes.

Domaines

Immunologie

Dates et versions

pasteur-00509601 , version 1 (13-08-2010)

Identifiants

Citer

Maria Elena Fernandez-Sanchez, Emmanuel Sechet, Florence Margottin-Goguet, Lars Rogge, Elisabetta Bianchi. The human COP9 signalosome protects ubiquitin-conjugating enzyme 3 (UBC3/Cdc34) from beta-transducin repeat-containing protein (betaTrCP)-mediated degradation.. Journal of Biological Chemistry, 2010, 285 (23), pp.17390-7. ⟨10.1074/jbc.M109.076661⟩. ⟨pasteur-00509601⟩
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