| A switch from p130Cas/Crk to Gab1/Crk signaling correlates with anchorage independent growth and JNK activation in cells transformed by the Met receptor oncoprotein. | None |
| Expression of the c-met proto-oncogene and its ligand, hepatocyte growth factor, in Hodgkin disease. | None |
| Immunohistochemical detection of the c-met proto-oncogene product in the congenital melanocytic nevus of an infant with neurocutaneous melanosis. | None |
| Structural basis of oncogenic activation caused by point mutations in the kinase domain of the MET proto-oncogene: modeling studies. | None |
| Receptor tyrosine kinases as therapeutic targets: the model of the MET oncogene. | None |
| Oncogenic mutants of RON and MET receptor tyrosine kinases cause activation of the beta-catenin pathway. | None |
| Role of the hepatocyte growth factor receptor, c-Met, in oncogenesis and potential for therapeutic inhibition | None |
| K252a inhibits the oncogenic properties of Met, the HGF receptor. | None |
| MET may be one of the long sought oncogenes controlling progression of primary cancers to metastasis. | None |
| Novel somatic mutations of the MET oncogene in human carcinoma metastases activating cell motility and invasion. | None |
| hepatocyte growth factor receptor, the product of the c-met protooncogene, is significantly suppressed by oxidative stress | None |
| Expression of c-met proto-oncogene in COS cells induces the signal transducing high-affinity receptor for hepatocyte growth factor. | None |
| Evidence for non-covalent clusters of the c-met proto-oncogene product. | None |
| Tumorigenicity of the met proto-oncogene and the gene for hepatocyte growth factor. | None |
| A novel small molecule met inhibitor induces apoptosis in cells transformed by the oncogenic TPR-MET tyrosine kinase. | None |
| Deregulated expression of interferon regulatory factor-1 in oncogene-transformed mouse fibroblasts. | None |
| A conserved DpYR motif in the juxtamembrane domain of the Met receptor family forms an atypical c-Cbl/Cbl-b tyrosine kinase binding domain binding site required for suppression of oncogenic activation. | None |
| Results provide an explanation for cell surface receptor cross-talk involving the Met receptor and link G protein-coupled receptors and the epidermal growth factor receptor to the oncogenic potential of Met signaling in human carcinoma cells. | None |
| Identification of C-met oncogene as a broadly expressed tumor-associated antigen recognized by cytotoxic T-lymphocytes. | None |
| c-Met oncogene is a novel tumor rejection antigen recognized by cytotoxic T-lymphocytes and expressed on a broad variety of epithelial and hematopoietic malignant cells | None |