Structural basis of oncogenic activation caused by point mutations in the kinase domain of the MET proto-oncogene: modeling studies.
Authors:
- 9 May 2001
- journal article
- research article
- Published by Wiley in Proteins: Structure, Function, and Bioinformatics
- Vol. 44 (1) , 32-43
Abstract
No abstract availableKeywords
This publication has 47 references indexed in Scilit:
- The Multisubstrate Docking Site of the MET Receptor Is Dispensable for MET-mediated RAS Signaling and Cell ScatteringMolecular Biology of the Cell, 1999
- Germline mutation of RET codon 883 in two cases of de novo MEN 2BOncogene, 1997
- Germline and somatic mutations in the tyrosine kinase domain of the MET proto-oncogene in papillary renal carcinomasNature Genetics, 1997
- C-kit mutations and mast cell disorders. A model of activating mutations of growth factor receptors.Hematology and Cell Therapy, 1997
- Interaction between Gab1 and the c-Met receptor tyrosine kinase is responsible for epithelial morphogenesisNature, 1996
- Hepatocyte growth factor/scatter factor—Met signaling in tumorigenicity and invasion/metastasisJournal of Molecular Medicine, 1996
- Mutation of juxtamembrane tyrosine residue 1001 suppresses loss-of-function mutations of the met receptor in epithelial cells.Proceedings of the National Academy of Sciences, 1995
- Placental defect and embryonic lethality in mice lacking hepatocyte growth factor/scatter factorNature, 1995
- Activation of RET as a Dominant Transforming Gene by Germline Mutations of MEN2A and MEN2BScience, 1995
- A multifunctional docking site mediates signaling and transformation by the hepatocyte growth factor/scatter factor receptor familyCell, 1994