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anti-Human MET Antibodies:
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Human Polyclonal MET Primary Antibody for BR, CyTOF - ABIN5012912
Skibinski, Elborn, Ennis: Bronchial epithelial cell growth regulation in fibroblast cocultures: the role of hepatocyte growth factor. in American journal of physiology. Lung cellular and molecular physiology 2007
Show all 17 Pubmed References
Human Polyclonal MET Primary Antibody for CyTOF, FACS - ABIN4900630
Phillip, Zaman, Shentu, Balakrishnan, Zhang, Baladandayuthapani, Taverna, Redkar, Wang, Stellrecht, Gandhi: Targeting MET kinase with the small-molecule inhibitor amuvatinib induces cytotoxicity in primary myeloma cells and cell lines. in Journal of hematology & oncology 2013
Show all 8 Pubmed References
Human Monoclonal MET Primary Antibody for FACS - ABIN4896926
Tervonen, Belitškin, Pant, Englund, Marques, Ala-Hongisto, Nevalaita, Sihto, Heikkilä, Leidenius, Hewitson, Ramachandra, Moilanen, Joensuu, Kovanen, Poso, Klefström: Deregulated hepsin protease activity confers oncogenicity by concomitantly augmenting HGF/MET signalling and disrupting epithelial cohesion. in Oncogene 2016
Show all 7 Pubmed References
Human Monoclonal MET Primary Antibody for FACS - ABIN4896921
Baccelli, Schneeweiss, Riethdorf, Stenzinger, Schillert, Vogel, Klein, Saini, Bäuerle, Wallwiener, Holland-Letz, Höfner, Sprick, Scharpff, Marmé, Sinn, Pantel, Weichert, Trumpp: Identification of a population of blood circulating tumor cells from breast cancer patients that initiates metastasis in a xenograft assay. in Nature biotechnology 2013
Show all 6 Pubmed References
Human Polyclonal MET Primary Antibody for ELISA (Detection), FACS - ABIN4899934
Coxon, Rex, Meyer, Sun, Sun, Chen, Radinsky, Kendall, Burgess: Soluble c-Met receptors inhibit phosphorylation of c-Met and growth of hepatocyte growth factor: c-Met-dependent tumors in animal models. in Molecular cancer therapeutics 2011
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Human Monoclonal MET Primary Antibody for CyTOF, FACS - ABIN4899935
Vogel, Börger, Peters, Förster, Liebfried, Metzger, Meisel, Däubener, Trapp, Fischer, Gawaz, Sorg: Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death. in Cell death and differentiation 2015
Show all 5 Pubmed References
Human Polyclonal MET Primary Antibody for FACS, IF (p) - ABIN671661
Gao, Bing, Li, Yang, Li, Chen: Study of critical role of c-Met and its inhibitor SU11274 in colorectal carcinoma. in Medical oncology (Northwood, London, England) 2013
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Human Polyclonal MET Primary Antibody for IHC - ABIN966572
Fan, Ma, Gao, Yuan, Meng, Goldberg, Rosen: The multisubstrate adapter Gab1 regulates hepatocyte growth factor (scatter factor)-c-Met signaling for cell survival and DNA repair. in Molecular and cellular biology 2001
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Human Polyclonal MET Primary Antibody for IHC (fro), ELISA - ABIN550491
Pavone, Cattaneo, Rea, De Pasquale, Spina, Sauchelli, Mastellone, Ammendola: Intracellular signaling cascades triggered by the NK1 fragment of hepatocyte growth factor in human prostate epithelial cell line PNT1A. in Cellular signalling 2011
Show all 4 Pubmed References
Human Polyclonal MET Primary Antibody for ELISA, WB - ABIN537686
Cattaneo, Parisi, Ammendola: WKYMVm-induced cross-talk between FPR2 and HGF receptor in human prostate epithelial cell line PNT1A. in FEBS letters 2013
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c-Met expression was revealed to be a useful marker for prognosis prediction in IDH-mutant lower-grade gliomas and glioblastoma
Gastric cancers that with positive c-MET expression had higher metabolic tumor volume and total lesion glycolysis compared with c-MET-negative gastric cancers. Volumetric parameters on 18F-FDG PET/CT may have a role in predicting prognosis of patients with c-MET-positive gastric cancer.
Knockdown of TUG1 through MET downregulation suppressed diffuse large B-cell lymphoma cell proliferation and tumor growth.
Study have established MET-amplified non-small cell lung cancer (NSCLC) cell lines that showed acquired resistance to capmatinib and evaluated its resistance mechanisms. Results demonstrated that capmatinib-resistant NSCLC cells were dependent on alternative pathway activation.
The present work seeks to assess whether pancreatic carcinomas release exosomes which express c-Met (proto-oncogene mesenchymal-epithelial transition factor) and PD-L1 (programmed cell death 1 ligand 1), and whether the detection of such expression in serum has diagnostic or prognostic meaning for the affected patients.
miR-34a may act as a suppressor in posterior capsule opacification by regulating human lens epithelial cell proliferation and migration through downregulation of c-Met.
these data were the first to demonstrate H. pylori infection-induced upregulation of activated MET in exosomes and the pro-tumorigenic effect on tumour-associated macrophages.
a membrane-bound retrograde vesicle transport mechanism facilitates membrane-to-nucleus transport of c-MET in breast cancer cells.
Anlotinib acts as a novel inhibitor of VEGFR2 and MET.
We found that both protein and gene expression levels of serum cMET, HGF and EGFR were higher in patients with lung cancer. We suggest that protein and gene expression levels of c-MET in patients with lung cancer will lead to targeted therapies as a new biomarker.
This is the first study from the Indian subcontinent to identify the frequency of ROS-1 re-arrangements and MET amplification in the Indian lung adenocarcinoma population. c-MET protein expression was identified in 33.33%, and ROS-1 protein expression was detected in 3.33% cases.
The review describes the role of MET signaling in gliomas, among which glioblastoma presents a major challenge with limited treatment options and poor prognosis. MET and its ligand HGF play a critical role in the proliferation, survival, migration, invasion, angiogenesis, stem cell characteristics, and therapeutic resistance and recurrence of glioblastomas. [review]
Seventeen publications involving a total of 1724 patients met the inclusion criteria. c-Met overexpression was significantly correlated with poor overall survival
High MET expression is associated with metastasis and tumor growth of lung adenocarcinoma.
findings suggest that lowintensity ultrasound could enhance the chemosensitivity of hepatocellular carcinoma cells to cisplatin by altering the miR34a/cMet axis.
Using patient-derived cell line and xenografts, we characterize the mechanism of crizotinib resistance mediated by KRAS amplification in METex14-mutant NSCLC and demonstrate the superior efficacy of the dual MET/PI3K inhibition as a therapeutic strategy addressing this resistance mechanism.
the role of lncRNA HOTAIR/miR-613/c-met signalling axis in modulating retinoblastoma cells' viability, apoptosis and expressions of EMT-specific proteins might provide evidences for developing appropriate diagnostic and treatment strategies for retinoblastoma.
The increased expression of HGF in CAFs induced by MET-unamplified GC.
We show that MET activation promotes the expression of several negative checkpoint regulators of the immunoresponse, including PD-L1. In addition, we report inactivation of JAK2 in lung cancer cells that prevented the response to IFNgamma.
elevated levels of urinary cMet at the time of initial diagnosis could predict renal outcomes in patients with diabetic nephropathy.
These results demonstrated hHGF gene transfer induced further overexpression of endogenous rHGF and c-Met mRNAs but lowered immunoreactivities of rHGF and c-Met in the neointima, thus leading to significant attenuation of neointimal hyperplasia.
Activation of hepatocyte growth factor/MET signaling initiates oncogenic transformation and enhances tumor aggressiveness in the murine prostate.
Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET.
High MET expression is associated with Oral Cancer.
High MET expression is associated with glioma brain invasion.
Data illustrateS a cooperative effect of the direct oncogenic signaling of mutant beta-catenin and MET in hepatocytes with hepatic tumor-promoting stroma induced by beta-catenin deficiency
Data indicate that c-met as a target for miR-146a in mouse model of colorectal cancer (CRC) liver metastasis (CLM).
Data provide the first evidence of spontaneous bleeding in Par4(-/-) mice, suggest that a dam's first litter provides a greater hemostatic challenge than subsequent litters.
PAR-4 is expressed in cardiac fibroblasts and is regulated by extracellular glucose and in diabetes mellitus.
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, 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.
SOCS1 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.
The data of this study suggest that MET+ neurons in the brainstem vagal motor nuclei are anatomically positioned to regulate distinct portions of the gastrointestinal tract.
Met has a role in promoting formation of double minute chromosomes induced by Sei-1 in NIH-3T3 murine fibroblasts
Malignant melanoma has the ability to undergo phenotypic change by a cell-intrinsic/autonomous mechanism that can be characterized by Met expression.
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).
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 complex.
MET signaling regulates intestinal homeostasis and regeneration, as well as adenoma formation. These activities of MET are promoted by the stem cell CD44 isoform CD44v4-10.
possible cooperative role of the EGF and HGF pathways and indicate that cross-talk between their respective receptors may modulate mammary gland development in the cow
HGF/c-Met signaling in neurons promotes axonal growth but suppresses filopodial assembly in neurons and hinders neuromuscular junction establishment.
Met receptor-mediated cell-cycle progression require Raf1 and phosphatidylinositol 3-kinase signaling.
In macaque, MET expression is restricted to the posterior cingulate, inferior temporal, posterior parietal, and visual cortices compared to mouse with broad neocortical distribution.
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
, hepatocyte growth factor receptor-like
, met proto-oncogene
, Proto-oncogene c-Met
, Scatter factor receptor
, Tyrosine-protein kinase Met
, Hepatocyte growth factor receptor
, HGF receptor c-Met
, proto-oncogene, receptor tyrosine kinase
, tyrosine kinase
, met proto-oncogene (hepatocyte growth factor receptor)
, MET proto-oncogene, receptor tyrosine kinase L homeolog
, c-met/hepatocyte growth factor receptor