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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 ELISA Kits) expression is associated with high c-MET expression, p16-negative tumors, and EGFR (show EGFR ELISA Kits)-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 ELISA Kits)-Tyrosine kinase (show TXK ELISA Kits) 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 ELISA Kits) T790M mutation.
revealed that salvianolic acid A enhanced sensitivity to cisplatin in A549/DDP (show TIMM8A ELISA Kits) cells mainly through suppression of the c-met/AKT (show AKT1 ELISA Kits)/mTOR (show FRAP1 ELISA Kits) signaling pathway
For intra-hepatic cholangiocarcinomas (IHCC)patients, ROS1 (show ROS1 ELISA Kits), ALK (show ALK ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) 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 as a key tumor suppressor of bladder cancer growth
Her2 (show ERBB2 ELISA Kits), cMet and FGFR2 (show FGFR2 ELISA Kits) statuses were profiled in gastric cancer (GC) patients and the -derived tumor xenograft(PDX) models.
Cells with ectopic FOXM1 (show FOXM1 ELISA Kits) expression demonstrate considerable ( approximately 20%, P < 0.001) growth advantage despite MET targeting.
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