Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
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
Data show that afatinib resistant clones were selectively killed by knock down of ERBB3 (show ERBB3 Proteins) + c-MET + c-KIT, but not by the individual or doublet knock down combinations, and the combination of afatinib with the SRC (show SRC Proteins) family inhibitor dasatinib killed afatinib resistant H1975 cells in a greater than additive fashion.
c-Met overexpression, HER-2 gene amplification, and SPTBN1-ALK gene fusion can coexist in lung adenocarcinoma and may become a potential biomarker of cancer refractory to crizotinib, chemotherapy, and radiotherapy as well as of a relatively poor prognosis.
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.
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 Proteins) and BRAF (show BRAF Proteins) dual/triple block combinations in BRAF (show BRAF Proteins)-mutated colorectal cancer. Switching from EGFR (show EGFR Proteins) to MET inhibition, while maintaining BRAF (show BRAF Proteins) inhibition, resulted in clinical benefit after the occurrence of MET-driven acquired resistance.
Which control critical events for colonization such as HGF (show HGF Proteins)/Met axis and Wwox (show WWOX Proteins), 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 Proteins) 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 Proteins)-MET fusion (ZM fusion).
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
c-Met has been found to attenuate lung injury and apoptosis in bronchial epithelial cells.
In this paper, we demonstrate a potential biochemical mechanism for such phenomena by showing that c-Met receptors promote the tyrosine phosphorylation of RalGDS (show RALGDS Proteins) at Y752 in its RBD (show CACNA1D Proteins), which blocks the binding of Ras to RalGDS (show RALGDS Proteins).
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