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MET levels were regulated by miR (show MLXIP ELISA Kits)-449b in TT cells. Together, we show that reduced miR (show MLXIP ELISA Kits)-449b levels in TT tissues may promote TC growth, through MET-mediated cell proliferation.
There are 2 categories of MET gene amplification in lung cancer patients, de novo and that secondary to TKI therapy. These patients can benefit from MET inhibitor therapy. Dual mechanisms of resistance, EGFR T790M mutation and c-MET amplification after TKI therapy, may suggest a poor prognosis.
MET amplification is here identified-clinically and preclinically-as a new mechanism of resistance to EGFR (show EGFR ELISA Kits) and BRAF (show BRAF ELISA Kits) dual/triple block combinations in BRAF (show BRAF ELISA Kits)-mutated colorectal cancer. Switching from EGFR (show EGFR ELISA Kits) to MET inhibition, while maintaining BRAF (show BRAF ELISA Kits) inhibition, resulted in clinical benefit after the occurrence of MET-driven acquired resistance.
Which control critical events for colonization such as HGF (show HGF ELISA Kits)/Met axis and Wwox (show WWOX ELISA Kits), as therapy of bone metastasis.
Data show that by reducing CD82, KSHV miR-K6-5p expedites cell invasion and angiogenesis by activating the c-Met pathway.
These results suggest MET overexpression is related to altered c-CBL (show CBL ELISA Kits) expression in head and neck squamous cell carcinoma, which may influence tumorigenesis
Authors characterized exosomes from GBM cells harbouring and not harbouring PTPRZ1 (show PTPRZ1 ELISA Kits)-MET fusion (ZM fusion).
Data demonstrated that c-Met activation increases miR (show MLXIP ELISA Kits)-130b levels, inhibits androgen receptor (show AR ELISA Kits) expression, promotes cancer spreading and resistance to hormone ablation therapy.
The role of the EGFR (show EGFR ELISA Kits) and Met interaction in glioblastoma.The role of MET in the glioblastoma resistance to treatment. [review]
NCTD suppressed not only the expression of the total EGFR and the phosphorylated EGFR but also the expression of the total c-Met.
possible cooperative role of the EGF (show EGF ELISA Kits) and HGF (show HGF ELISA Kits) 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
, hepatocyte growth factor
, hepatoCyte growth factor receptor
, met proto-oncogene
, Hepatocyte growth factor receptor
, hepatocyte growth factor receptor-like
, Proto-oncogene c-Met
, Scatter factor receptor
, Tyrosine-protein kinase Met