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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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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 (显示 STAT6 蛋白) phosphorylation occurs in response to MET activation in epithelial cells. However, STAT6 (显示 STAT6 蛋白) nuclear translocation does not occur in response to HGF (显示 HGF 蛋白), precluding the transcriptional activity of STAT6 (显示 STAT6 蛋白).
c-Met-activated Mesenchymal Stem Cells (MSC (显示 MSC 蛋白)) pre-exposed to hypoxia interact with PrPC (显示 PRNP 蛋白) at the site of ischemic injury to increase the efficiency of MSC (显示 MSC 蛋白) transplantation.
This study demonstrates that simultaneous inhibition of c-Met and Src (显示 SRC 蛋白) signaling in MD-MSCs triggers apoptosis and reveals vulnerable pathways that could be exploited to develop NF2 (显示 NF2 蛋白) therapies.
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 (显示 SHH 蛋白), 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.
We identified unique and tumor-specific tyrosine phosphorylation rewiring in tumors resistant to treatment with the irreversible third-generation EGFR (显示 EGFR 蛋白)-inhibitor, osimertinib, or the novel dual-targeting EGFR (显示 EGFR 蛋白)/Met antibody, JNJ-61186372.
TGF-beta (显示 TGFB1 蛋白) negatively controls the HGF/c-MET pathway by regulating of stemness in glioblastoma.
the results of real-time PCR and western blotting revealed that Huaier extract decreased p65 and c-Met expression and increased IkappaBalpha expression, while paclitaxel increased p65 expression and reduced IkappaBalpha and c-Met expression.The molecular mechanisms may be involved in the inhibition of the NF-kappaB pathway and c-Met expression
Data found that the expression of c-Met was significantly increased in human oral squamous cell carcinoma (OSCC) tissues than in normal mucosa adjacent to the tumor, but was not correlated with clinicopathological parameters. Also, further findings indicated the potential role of c-Met in the progression of OSCC.
Our data show that S49076 exerts its cytotoxic activity at low doses on MET-dependent cells through MET inhibition, whereas it inhibits growth of MET-independent cells at higher but clinically relevant doses by targeting Aurora B (显示 AURKB 蛋白)
In SCCHN, immunohistochemical overexpression of c-MET above cut-off levels III and particularly II was associated with inferior survival outcomes and advanced disease
PAR-4 (显示 F2RL3 蛋白) is expressed in cardiac fibroblasts and is regulated by extracellular glucose and in diabetes mellitus.
SOCS1 (显示 SOCS1 蛋白) 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.
Met has a role in promoting formation of double minute chromosomes induced by Sei-1 (显示 SERTAD1 蛋白) 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 (显示 EGFR 蛋白)).
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 (显示 CTNNB1 蛋白) complex.
possible cooperative role of the EGF (显示 EGF 蛋白) and HGF (显示 HGF 蛋白) 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