Structural basis of oncogenic activation caused by point mutations in the kinase domain of the MET proto-oncogene: Modeling studies
Author:
Publisher
Wiley
Subject
Molecular Biology,Biochemistry,Structural Biology
Reference51 articles.
1. A multifunctional docking site mediates signaling and transformation by the hepatocyte growth factor/scatter factor receptor family
2. Mutation of juxtamembrane tyrosine residue 1001 suppresses loss-of-function mutations of the met receptor in epithelial cells.
3. The Multisubstrate Docking Site of the MET Receptor Is Dispensable for MET-mediated RAS Signaling and Cell Scattering
4. Interaction between Gab1 and the c-Met receptor tyrosine kinase is responsible for epithelial morphogenesis
5. Placental defect and embryonic lethality in mice lacking hepatocyte growth factor/scatter factor
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