| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10763302 | Biochemical and Biophysical Research Communications | 2011 | 6 Pages |
Abstract
⺠Upon hepatocyte growth factor/scatter factor (HGF/SF) induced MET tyrosine kinase receptor activation, the GAB1 adaptor is degraded by the proteasome. ⺠GAB1 is recruited by the activated MET receptor which in turn induces GAB1 ubiquitination. ⺠GAB1 is ubiquitinated in a CBL-dependent manner. ⺠Ligand-induced GAB1 degradation hampers downstream activation of ERK MAP kinases upon MET rechallenge. ⺠Down-regulation of GAB1 is a negative feedback mechanism in HGF/SF-MET signaling.
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Authors
Gautier Goormachtigh, Zongling Ji, Arnaud Le Goff, Véronique Fafeur,