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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
Show all 7 Pubmed References
RAS mutations and HER2 (show ERBB2 Proteins)/MET amplification were the most frequently detected resistance mechanisms in both tissue and blood sample analysis. On the other hand, BRAF (show BRAF Proteins) and EGFR (show EGFR Proteins) ectodomain mutations were much rarer.The combined analysis of tissue and blood (ctDNA) results highlights the complexity of clonal evolution triggered by EGFR (show EGFR Proteins) blockade
Findings suggest that MET rs1621 polymorphism, alone and combined with miR (show MLXIP Proteins)-199a rs74723057, may influence susceptibility to hepatocellular carcinoma.
ABBV-399 represents a novel therapeutic strategy to deliver a potent cytotoxin to c-Met-overexpressing tumor cells enabling cell killing regardless of reliance on MET signaling. ABBV-399 has progressed to a phase I study where it has been well tolerated and has produced objective responses in c-Met-expressing non-small cell lung cancer (NSCLC) patients.
High CD44 (show CD44 Proteins) expression is associated with high c-MET expression, p16-negative tumors, and EGFR (show EGFR Proteins)-positive tumors. The combination of these markers predicts for poor prognosis in HNSCC patients treated with chemoradiation.
MET/T790M-positive patients are at higher risk of acquired resistance to EGFR (show EGFR Proteins)-Tyrosine kinase (show TXK Proteins) inhibitors, and have a worse Post-progression survival than patients with only MET overexpression or the T790M mutation alone. Clinical trials are needed to determine the best treatment for patients with both MET overexpression and the EGFR (show EGFR Proteins) T790M mutation.
revealed that salvianolic acid A enhanced sensitivity to cisplatin in A549/DDP (show TIMM8A Proteins) cells mainly through suppression of the c-met/AKT (show AKT1 Proteins)/mTOR (show FRAP1 Proteins) signaling pathway
For intra-hepatic cholangiocarcinomas (IHCC)patients, ROS1 (show ROS1 Proteins), ALK and c-MET expression levels have prognostic significance on clinical outcomes. Although this finding may require further validation, it has led to proposal of a new stratification or enriched biomarker for future phase III trial of anti-EGFR (show EGFR Proteins) therapy in IHCC.
Data show that MET amplification identified by circulating-free DNA (cfDNA) occurred in a sizable subset of patients that are refractory to anti-EGFR (show EGFR Proteins) therapy.
Data suggest palmitoylation is required for egress from the Golgi for transport to the plasma membrane. These findings introduce palmitoylation as a critical modification of c-Met.
our studies for the first time establish p100 (show CUX1 Proteins) as a key tumor suppressor of bladder cancer growth
Met has a role in promoting formation of double minute chromosomes induced by Sei-1 (show SERTAD1 Proteins) in NIH-3T3 murine fibroblasts
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 (show EGFR Proteins)).
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 (show CTNNB1 Proteins) complex.
MET signaling regulates intestinal homeostasis and regeneration, as well as adenoma formation. These activities of MET are promoted by the stem cell CD44 (show CD44 Proteins) isoform CD44v4-10.
a c-Met/ETS-1 (show ETS1 Proteins)/matrix metalloproteinase-14 (MMP-14 (show MMP14 Proteins)) axis that controls VE-cadherin (show CDH5 Proteins) degradation, endothelial mesenchymal transition, and vascular abnormality.
We found the roles of hepatocyte growth factor (HGF (show HGF Proteins)) signaling in stria vascularis development for the first time and that lack of HGF (show HGF Proteins) 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 (show HGF Proteins) and DFNB97. Our findings reveal an additional example of context-dependent c-MET signaling diversity, required here for proper cellular inva
possible cooperative role of the EGF (show EGF Proteins) and HGF (show HGF Proteins) pathways and indicate that cross-talk between their respective receptors may modulate mammary gland development in the cow
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
, HGF receptor c-Met