Degradation of the GAB1 adaptor by the ubiquitin-proteasome pathway hampers HGF/SF-MET signaling

Biochem Biophys Res Commun. 2011 Aug 12;411(4):780-5. doi: 10.1016/j.bbrc.2011.07.024. Epub 2011 Jul 18.

Abstract

The GRB2 associated binder 1 (GAB1) is an essential docking/adaptor protein for transmitting intracellular signals of the MET tyrosine kinase receptor activated by hepatocyte growth factor/scatter factor (HGF/SF). We found that in response to hours of HGF/SF treatment, the GAB1 protein level is degraded by a mechanism involving MET activity and the proteasomal machinery. We also showed that GAB1 is both multi- and poly-ubiquitinated in a CBL-dependent manner. A long term exposure to HGF/SF caused a more sustained down-regulation of GAB1 than of MET, associated with a loss of reactivation of the ERK MAP kinases to subsequent acute ligand treatment. These data demonstrate that GAB1 is ubiquitinated by CBL and degraded by the proteasome, and plays a role in negative-feedback regulation of HGF/SF-MET signaling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism*
  • HEK293 Cells
  • HeLa Cells
  • Hepatocyte Growth Factor / metabolism*
  • Humans
  • Proteasome Endopeptidase Complex / metabolism*
  • Proto-Oncogene Proteins c-cbl / metabolism
  • Proto-Oncogene Proteins c-met / metabolism*
  • Receptors, Growth Factor / metabolism*
  • Signal Transduction
  • Ubiquitin / metabolism
  • Ubiquitination*

Substances

  • Adaptor Proteins, Signal Transducing
  • GAB1 protein, human
  • HGF protein, human
  • Receptors, Growth Factor
  • Ubiquitin
  • Hepatocyte Growth Factor
  • Proto-Oncogene Proteins c-cbl
  • MET protein, human
  • Proto-Oncogene Proteins c-met
  • Proteasome Endopeptidase Complex
  • CBL protein, human