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Human MET Protein expressed in Human Cells - ABIN2003241
Bottaro, Rubin, Faletto, Chan, Kmiecik, Vande Woude, Aaronson: Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product. in Science (New York, N.Y.) 1991
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the miR-19a/c-Met pathway plays a critical role in acquired resistance to gefitinib and that the manipulation of miR-19a might provide a therapeutic strategy for overcoming acquired gefitinib resistance.
The expression of C-Met and HER2 protein in lung adenocarcinoma is highly correlated, and whether it is synergistic in the targeted therapy of lung adenocarcinoma deserves further study.
MET overexpression was more frequently found in high grade myxofibrosarcoma and the epithelioid variant. Chromosome 7 polysomy, rather than MET gene regional amplification, might account for the overexpression. of MET protein.
miR-449a suppresses hepatocellular carcinoma tumorigenesis by down-regulating activity in the c-Met/ERK pathway.
We found MET amplifications in two cases of endometrial clear-cell carcinoma with mixed features.
Regarding gene mutation abundance, NGS enables the detection of low-abundant ctDNA in blood based on ultra-deep sequencing, and our patient benefited from crizotinib despite the low abundance of MET exon 14 skipping. These data indicate that we can choose targeted therapy despite the low abundance of gene mutations.
The interplay of dual MET/HER2 overexpression in the AKT and ERK pathways for esophageal cancer is described. Therefore, combination therapy could be a novel strategy for EAC with amplification of both MET and HER2.
MET inactivation in the context of the BRAF-activating mutation is driven through a negative feedback loop involving inactivation of PP2A phosphatase, which in turn leads to phosphorylation on MET inhibitory Ser985.
MET Exon 14 Skipping Mutations in Non-small Cell Lung Cancer
MET activation, by either METex14 mutations or amplification, is characteristic of a subset of early stage NSCLCs and may coexist with ERBB2 amplification.
Results demonstrate that serum level of miR-658 is significantly lower in the NM group than in the DM group. Meanwhile, the levels of PAX3 and MET are lower in the NM group than in the DM group too. Both overexpression and silence of miR-658 significantly up-regulate or down-regulate the levels of PAX3 and MET in gastric cell lines.
MiR-206 inhibits the development of epithelial ovarian cancer cell by directly targeting c-Met and inhibiting the c-Met/AKT/mTOR signaling pathway.
These results suggest that gastric cancer progression is not associated with a unique signaling pathway and that a feedback loop may exist between the HGF/c-Met and Notch1 signaling pathways, which may result in therapeutic resistance.
Comparative analysis revealed a strong association between MET expression and MET amplification (85% concurrence) in primary stomach tumors and matched liver metastasis. Survival analyses revealed that both MET amplification and MET overexpression were prognostic of poor outcomes.
High c-met expression is associated with oral squamous cell carcinoma.
FOXO1 serves as an important linker between HER2 and MET signaling pathways through negative crosstalks and is a key regulator of the acquired lapatinib resistance in HER2-positive GC cells.
analysis of how the cMET blockade augments radiation therapy in patients with NF2
these findings highlight the relevance of cross-species protein interactions between murine feeder cells and human epithelial cells in 3T3-J2 co-culture and demonstrate that STAT6 phosphorylation occurs in response to MET activation in epithelial cells. However, STAT6 nuclear translocation does not occur in response to HGF, precluding the transcriptional activity of STAT6.
c-Met-activated Mesenchymal Stem Cells (MSC) pre-exposed to hypoxia interact with PrPC at the site of ischemic injury to increase the efficiency of MSC transplantation.
A novel G-quadruplex motif formed in the Human MET promoter region.
Data illustrateS a cooperative effect of the direct oncogenic signaling of mutant beta-catenin and MET in hepatocytes with hepatic tumor-promoting stroma induced by beta-catenin deficiency
Data indicate that c-met as a target for miR-146a in mouse model of colorectal cancer (CRC) liver metastasis (CLM).
Data provide the first evidence of spontaneous bleeding in Par4(-/-) mice, suggest that a dam's first litter provides a greater hemostatic challenge than subsequent litters.
PAR-4 is expressed in cardiac fibroblasts and is regulated by extracellular glucose and in diabetes mellitus.
prolonged treatment of single HGF/c-Met or Hh inhibitor leads to resistance to these single inhibitors, likely because the single c-Met treatment leads to enhanced expression of Shh, and vice versa. Targeting both the HGF/c-Met and Hh pathways simultaneously overcame the resistance to the single-inhibitor treatment and led to a more potent antitumor effect in combination with the chemotherapy treatment.
SOCS1 attenuates migration and invasion properties of hepatocellular carcinoma cells at least partly via modulation of MET-mediated epithelial-mesenchymal transition, and controls invasive tumor growth.
The data of this study suggest that MET+ neurons in the brainstem vagal motor nuclei are anatomically positioned to regulate distinct portions of the gastrointestinal tract.
Met has a role in promoting formation of double minute chromosomes induced by Sei-1 in NIH-3T3 murine fibroblasts
Malignant melanoma has the ability to undergo phenotypic change by a cell-intrinsic/autonomous mechanism that can be characterized by Met expression.
Genetic activation of the antioxidant transcription factor Nrf2 improves liver damage and repair in hepatocyte-specific c-met-deficient mice mainly through restoring a balance in the cellular redox homeostasis.
MET promoted the development of squamous tumors by stimulating the synthesis and release of ligands that activate the epidermal growth factor receptor (EGFR).
through the activation of EGFR, MET activation parallels a RAS pathway to contribute to human and mouse cutaneous cancers.
Results show that c-MET expression is significantly low in pancreatic neuroendocrine tumors (PNETs) and is under the regulation of Meg3-mediated transcriptional and epigenetic mechanisms which contributes to the pathogenesis of PNETs.
Findings indicate a role for the hepatocyte growth factor receptor HGFR/c-MET pathway in neutrophil recruitment and function and suggest that c-MET inhibitor co-treatment may improve responses to cancer immunotherapy in settings beyond c-MET-dependent tumors.
Results demonstrate a new mechanism for the modulation of synapse formation, whereby MET activation induces an alignment of presynaptic and postsynaptic elements that are necessary for assembly and formation of functional synapses by subsets of neocortical neurons that express MET/beta-catenin complex.
MET signaling regulates intestinal homeostasis and regeneration, as well as adenoma formation. These activities of MET are promoted by the stem cell CD44 isoform CD44v4-10.
Study examined the signaling mechanisms through which MET exerts developmental effects in the neocortex. Data reveal a key role for MET activation during the period of neocortical neuron growth and synaptogenesis, with distinct biological outcomes mediated via discrete MET-linked intracellular signaling pathways in the same neurons.
a c-Met/ETS-1/matrix metalloproteinase-14 (MMP-14) axis that controls VE-cadherin degradation, endothelial mesenchymal transition, and vascular abnormality.
We found the roles of hepatocyte growth factor (HGF) signaling in stria vascularis development for the first time and that lack of HGF signaling in the inner ear leads to profound hearing loss in the mouse. Our findings reveal a novel mechanism that may underlie human deafness DFNB39 and DFNB97. Our findings reveal an additional example of context-dependent c-MET signaling diversity, required here for proper cellular inva
c-Met has been found to attenuate lung injury and apoptosis in bronchial epithelial cells.
possible cooperative role of the EGF and HGF pathways and indicate that cross-talk between their respective receptors may modulate mammary gland development in the cow
HGF/c-Met signaling in neurons promotes axonal growth but suppresses filopodial assembly in neurons and hinders neuromuscular junction establishment.
Met receptor-mediated cell-cycle progression require Raf1 and phosphatidylinositol 3-kinase signaling.
In macaque, MET expression is restricted to the posterior cingulate, inferior temporal, posterior parietal, and visual cortices compared to mouse with broad neocortical distribution.
The proto-oncogene MET product is the hepatocyte growth factor receptor and encodes tyrosine-kinase activity. The primary single chain precursor protein is post-translationally cleaved to produce the alpha and beta subunits, which are disulfide linked to form the mature receptor. Various mutations in the MET gene are associated with papillary renal carcinoma. Two transcript variants encoding different isoforms have been found for this gene.
, HGF/SF receptor
, SF receptor
, hepatocyte growth factor receptor
, met proto-oncogene tyrosine kinase
, proto-oncogene c-Met
, scatter factor receptor
, tyrosine-protein kinase Met
, hepatocyte growth factor receptor-like
, met proto-oncogene
, Proto-oncogene c-Met
, Scatter factor receptor
, Tyrosine-protein kinase Met
, Hepatocyte growth factor receptor
, HGF receptor c-Met
, proto-oncogene, receptor tyrosine kinase
, tyrosine kinase
, met proto-oncogene (hepatocyte growth factor receptor)
, MET proto-oncogene, receptor tyrosine kinase L homeolog
, c-met/hepatocyte growth factor receptor