Pathway specificity for Met signalling
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Summary
Signals generated by the tyrosine kinase receptor Met elicit a complex biological response including cell dissociation, migration, protection from apoptosis, proliferation and differentiation, showing that there is specificity in intracellular pathways.
- Type
- article
- Published
- 2001-07-01
- Cited by
- 99
- References
- 16
- OpenAlex
- https://openalex.org/W1578039249
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:11725384
Keywords
Phosphorylation, Cell biology, Tyrosine, Tyrosine phosphorylation, Receptor tyrosine kinase
References
- Oncogenic kinase signalling
- Induction of epithelial tubules by growth factor HGF depends on the STAT pathway
- Specific Uncoupling of GRB2 from the Met Receptor
- Uncoupling of Grb2 from the Met receptor in vivo reveals complex roles in muscle development.
- A multifunctional docking site mediates signaling and transformation by the hepatocyte growth factor/scatter factor receptor family.
- Phosphoinositide 3-Kinase Induces Scattering and Tubulogenesis in Epithelial Cells through a Novel Pathway*
- Interaction between Gab1 and the c-Met receptor tyrosine kinase is responsible for epithelial morphogenesis
- Developmental roles of HGF/SF and its receptor, the c-Met tyrosine kinase.
- Scatter factors and invasive growth.
- Coupling Met to specific pathways results in distinct developmental outcomes.
- Protein-protein interactions define specificity in signal transduction.
- Uncoupling signal transducers from oncogenic MET mutants abrogates cell transformation and inhibits invasive growth.
- Diverse signaling pathways activated by growth factor receptors induce broadly overlapping, rather than independent, sets of genes.
- Constitutive activation of the RON gene promotes invasive growth but not transformation
- A point mutation in the MET oncogene abrogates metastasis without affecting transformation.
- Sustained recruitment of phospholipase C-γ to Gab1 is required for HGF-induced branching tubulogenesis
Cited by
- MetMAb, the one-armed 5D5 anti-c-Met antibody, inhibits orthotopic pancreatic tumor growth and improves survival.
- ADAM10/17-dependent release of soluble c-Met correlates with hepatocellular damage.
- An orally available small-molecule inhibitor of c-Met, PF-2341066, reduces tumor burden and metastasis in a preclinical model of ovarian cancer metastasis.
- c-Met: Structure, functions and potential for therapeutic inhibition
- Liver regeneration--the best kept secret. A model of tissue injury response.
- Study of inflammatory signalling in epithelial ovarian cancer and the normal human mesothelium
- Principles of Liver Regeneration and Growth Homeostasis
- MET inhibition in lung cancer.
- The role of JNK2 and JNK1 in breast cancer mediated invasion and metastasis
- Role of MET in SV40-induced mammary tumorigenesis
- Met-Independent Hepatocyte Growth Factor-mediated regulation of cell adhesion in human prostate cancer cells
- Hepatocyte Growth Factor Induces Glucose Uptake in 3T3-L1 Adipocytes through A Gab1/Phosphatidylinositol 3-Kinase/Glut4 Pathway*
- Serum and tissue biomarkers as predictive and prognostic variables in epithelial ovarian cancer.
- Downstream signalling and specific inhibition of c-MET/HGF pathway in small cell lung cancer: implications for tumour invasion
- Met-HGF/SF signal transduction induces mimp, a novel mitochondrial carrier homologue, which leads to mitochondrial depolarization.
- Definition of a direct extracellular interaction between Met and E‐cadherin
- AXL and MET Crosstalk to Promote Gonadotropin Releasing Hormone (GnRH) Neuronal Cell Migration and Survival
- KRC-327, a selective novel inhibitor of c-Met receptor tyrosine kinase with anticancer activity.
- Oncogenes as Novel Targets for Cancer Therapy (Part I)
- Molecular biology of renal cell cancer and the identification of therapeutic targets.
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