Name: Recombinant Human Hepatocyte growth factor receptor(MET),partial (Active)
Brand: CUSABIO
SKU: CSB-MP013714HU

Product Details

Description	Recombinant human hepatocyte growth factor receptor (MET) carrying a C-terminal hFc-tag is a partial-length protein expressed in mammalian cells. The DNA fragment used to prepare this recombinant MET protein corresponds to amino acid residues Glu25-Thr932 of the human MET protein. Its purity is greater than 90% determined by SDS-PAGE. A molecular mass band of approximately 100-116 kDa was visualized on the gel. The endotoxin of this recombinant MET protein is less than 1.0 EU/ug measured by the LAL method. It has been validated as an active protein. In the function ELISA, this MET protein can bind to the anti-MET antibody with the EC₅₀ of 2.379-3.094 ng/ml. And it is available now. MET binds to its cognate ligand the hepatocyte growth factor (HGF) and is activated to induce various biological responses, including proliferation, motility, cell survival, morphogenesis, and angiogenesis. The HGF-MET signaling pathway is also involved in the development of the epithelial organs, exerts regenerative effects on the epithelium, and promotes the regression of fibrosis in numerous organs. Studies have shown that the HGF-MET signaling pathway is associated with the biology of cancer types, neurons, and immunity.
Purity	Greater than 90% as determined by SDS-PAGE.
Endotoxin	Less than 1.0 EU/ug as determined by LAL method.
Activity	①Measured by its binding ability in a functional ELISA. Immobilized MET at 2 μg/ml can bind Anti-MET recombinant antibody, the EC₅₀ is 2.379-3.094 ng/ml.
Target Names	MET
Uniprot No.	P08581
Research Area	Cancer
Alternative Names	(HGF receptor)(HGF/SF receptor)(Proto-oncogene c-Met)(Scatter factor receptor)(SF receptor)(Tyrosine-protein kinase Met)
Molecular Characterization
Species	Homo sapiens (Human)
Source	Mammalian cell
Expression Region	25-932aa
Target Protein Sequence	ECKEALAKSEMNVNMKYQLPNFTAETPIQNVILHEHHIFLGATNYIYVLNEEDLQKVAEYKTGPVLEHPDCFPCQDCSSKANLSGGVWKDNINMALVVDTYYDDQLISCGSVNRGTCQRHVFPHNHTADIQSEVHCIFSPQIEEPSQCPDCVVSALGAKVLSSVKDRFINFFVGNTINSSYFPDHPLHSISVRRLKETKDGFMFLTDQSYIDVLPEFRDSYPIKYVHAFESNNFIYFLTVQRETLDAQTFHTRIIRFCSINSGLHSYMEMPLECILTEKRKKRSTKKEVFNILQAAYVSKPGAQLARQIGASLNDDILFGVFAQSKPDSAEPMDRSAMCAFPIKYVNDFFNKIVNKNNVRCLQHFYGPNHEHCFNRTLLRNSSGCEARRDEYRTEFTTALQRVDLFMGQFSEVLLTSISTFIKGDLTIANLGTSEGRFMQVVVSRSGPSTPHVNFLLDSHPVSPEVIVEHTLNQNGYTLVITGKKITKIPLNGLGCRHFQSCSQCLSAPPFVQCGWCHDKCVRSEECLSGTWTQQICLPAIYKVFPNSAPLEGGTRLTICGWDFGFRRNNKFDLKKTRVLLGNESCTLTLSESTMNTLKCTVGPAMNKHFNMSIIISNGHGTTQYSTFSYVDPVITSISPKYGPMAGGTLLTLTGNYLNSGNSRHISIGGKTCTLKSVSNSILECYTPAQTISTEFAVKLKIDLANRETSIFSYREDPIVYEIHPTKSFISGGSTITGVGKNLNSVSVPRMVINVHEAGRNFTVACQHRSNSEIICCTTPSLQQLNLQLPLKTKAFFMLDGILSKYFDLIYVHNPVFKPFEKPVMISMGNENVLEIKGNDIDPEAVKGEVLKVGNKSCENIHLHSEAVLCTVPNDLLKLNSELNIEWKQAISSTVLGKVIVQPDQNFT
Mol. Weight	130.6 kDa
Protein Length	Partial
Tag Info	C-terminal hFc-tagged
Form	Lyophilized powder Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer	Lyophilized from a 0.2 μm filtered PBS, 6% Trehalose, pH 7.4
Reconstitution	We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs	Protein FAQs
Storage Condition	Store at -20°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life	The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time	3-7 business days
Notes	Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA	Please contact us to get it.

Target Background

Function (From Uniprot)	Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells. May regulate cortical bone osteogenesis (By similarity).
Gene References into Functions	the miR-19a/c-Met pathway plays a critical role in acquired resistance to gefitinib and that the manipulation of miR-19a might provide a therapeutic strategy for overcoming acquired gefitinib resistance. PMID: 28592790 The expression of C-Met and HER2 protein in lung adenocarcinoma is highly correlated, and whether it is synergistic in the targeted therapy of lung adenocarcinoma deserves further study. PMID: 29400000 MET overexpression was more frequently found in high grade myxofibrosarcoma and the epithelioid variant. Chromosome 7 polysomy, rather than MET gene regional amplification, might account for the overexpression. of MET protein. PMID: 30126419 miR-449a suppresses hepatocellular carcinoma tumorigenesis by down-regulating activity in the c-Met/ERK pathway. PMID: 30108016 We found MET amplifications in two cases of endometrial clear-cell carcinoma with mixed features. PMID: 29633423 Regarding gene mutation abundance, NGS enables the detection of low-abundant ctDNA in blood based on ultra-deep sequencing, and our patient benefited from crizotinib despite the low abundance of MET exon 14 skipping. These data indicate that we can choose targeted therapy despite the low abundance of gene mutations. PMID: 29110851 The interplay of dual MET/HER2 overexpression in the AKT and ERK pathways for esophageal cancer is described. Therefore, combination therapy could be a novel strategy for EAC with amplification of both MET and HER2. PMID: 29223420 MET inactivation in the context of the BRAF-activating mutation is driven through a negative feedback loop involving inactivation of PP2A phosphatase, which in turn leads to phosphorylation on MET inhibitory Ser985. PMID: 30224486 MET Exon 14 Skipping Mutations in Non-small Cell Lung Cancer PMID: 30037377 MET activation, by either METex14 mutations or amplification, is characteristic of a subset of early stage NSCLCs and may coexist with ERBB2 amplification. PMID: 29139039 Results demonstrate that serum level of miR-658 is significantly lower in the NM group than in the DM group. Meanwhile, the levels of PAX3 and MET are lower in the NM group than in the DM group too. Both overexpression and silence of miR-658 significantly up-regulate or down-regulate the levels of PAX3 and MET in gastric cell lines. PMID: 29630524 MiR-206 inhibits the development of epithelial ovarian cancer cell by directly targeting c-Met and inhibiting the c-Met/AKT/mTOR signaling pathway. PMID: 29807226 These results suggest that gastric cancer progression is not associated with a unique signaling pathway and that a feedback loop may exist between the HGF/c-Met and Notch1 signaling pathways, which may result in therapeutic resistance. PMID: 29781036 Comparative analysis revealed a strong association between MET expression and MET amplification (85% concurrence) in primary stomach tumors and matched liver metastasis. Survival analyses revealed that both MET amplification and MET overexpression were prognostic of poor outcomes. PMID: 29790169 High c-met expression is associated with oral squamous cell carcinoma. PMID: 29286169 FOXO1 serves as an important linker between HER2 and MET signaling pathways through negative crosstalks and is a key regulator of the acquired lapatinib resistance in HER2-positive GC cells. PMID: 28343375 analysis of how the cMET blockade augments radiation therapy in patients with NF2 PMID: 29440379 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 phosphorylation occurs in response to MET activation in epithelial cells. However, STAT6 nuclear translocation does not occur in response to HGF, precluding the transcriptional activity of STAT6. PMID: 29771943 c-Met-activated Mesenchymal Stem Cells (MSC) pre-exposed to hypoxia interact with PrPC at the site of ischemic injury to increase the efficiency of MSC transplantation. PMID: 29705776 A novel G-quadruplex motif formed in the Human MET promoter region. PMID: 29054971 a METex14 del mutation-positive NSCLC patient who responded to crizotinib but later relapsed, demonstrated a mixed response to glesatinib including reduction in size of a MET Y1230H mutation-positive liver metastasis and concurrent loss of detection of this mutation in plasma DNA. Together, these data demonstrate that glesatinib exhibits a distinct mechanism of target inhibition and can overcome resistance to PMID: 28765324 This study demonstrates that simultaneous inhibition of c-Met and Src signaling in MD-MSCs triggers apoptosis and reveals vulnerable pathways that could be exploited to develop NF2 therapies. PMID: 28775147 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. PMID: 28864680 We identified unique and tumor-specific tyrosine phosphorylation rewiring in tumors resistant to treatment with the irreversible third-generation EGFR-inhibitor, osimertinib, or the novel dual-targeting EGFR/Met antibody, JNJ-61186372. PMID: 28830985 TGF-beta negatively controls the HGF/c-MET pathway by regulating of stemness in glioblastoma. PMID: 29238047 The preclinical efficacy and safety data provide a clear rationale for the ongoing clinical studies of Sym015 in patients with MET-amplified tumors. PMID: 28679766 High MET expression is associated with malignant pleural mesothelioma. PMID: 28560410 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 PMID: 29039556 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. PMID: 29115556 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 PMID: 28619752 MET expression was shown to be significantly reduced in the superior temporal gyrus cortex of autism spectrum disorders individuals. PMID: 28322981 In SCCHN, immunohistochemical overexpression of c-MET above cut-off levels III and particularly II was associated with inferior survival outcomes and advanced disease PMID: 29103754 Here we present a case series of three such patients who achieved were cMET amplified and showed partial response on Crizotinib PMID: 29199685 c-Met/beta1 integrin complex whose ligand-independent cross-activation and robust affinity for fibronectin drives invasive oncologic processes. PMID: 28973887 tivantinib did not suppress MET signaling, and selective MET inhibitors demonstrated an antiproliferative effect only in MHCC97H, the unique cell line displaying MET gene amplification. HCC tumors with high expression of cell proliferation genes defined a group of patients with poor survival. PMID: 28246274 Studies show that MET mutations have been found in cancer of unknown primary origin (CUP) being clustered to the SEMA and TK domain of the receptor. The biomechanical properties of MET mutants might trigger the hyper-invasive phenotype associated to CUP. [review] PMID: 29037604 Data show that Kruppel like factor 4 (KLF4) was overexpressed in met proto-oncogene protein (c-Met)-overexpressing non-small-cell lung cancer (NSCLC) cells and tissues. PMID: 29624806 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. PMID: 29085209 The authors reconfirmed EGFR mutation as a strong predictive marker of Non-Small-Cell Lung Cancer. However, c-MET positivity was not associated with response or progression-free survival, although c-MET overexpression correlated with some clinical characteristics. PMID: 29502124 findings show oncogene E5 is primarily responsible for Met upregulation; E5-induced Met contributes motility of HPV-containing cells; these studies show a new role for E5 in epithelial-stromal interactions, with implications for cancer development PMID: 29609071 EGFR T790M mutation and cMET amplification are main mechanisms leading to EGFR TKI resistance in lung adenocarcinoma. PMID: 29616327 MET activation is associated with drug resistance in chronic myeloid leukemia. PMID: 28418880 High glucose activated Met receptor in HK2 cells independently of HGF, via induction of integrin a5b1 and downstream signaling. This mode of Met activation was associated with tubular cell damage and apoptosis and it may represent a novel pathogenic mechanism and a treatment target in diabetic nephropathy. PMID: 28819999 The purpose of this study was to explore gene copy number (GCN) variation of EGFR, HER2, c-MYC, and MET in patients with primary colorectal cancer. PMID: 28764718 HGF/c-MET pathway mediates VEGFR inhibitor resistance and vascular remodeling in NSCLC. PMID: 28559461 Because c-Met is strongly associated with pathological grade, stage and disease-specific survival, c-Met levels may have potential to predict patient prognosis and to guide clinical diagnosis and treatment of patients with renal cell carcinoma PMID: 28427859 miR-1 is downregulated in ovarian cancer tissues, and may play a tumor suppressive role by inhibiting c-Met expression and its effects on the regulation of cell proliferation, migration and invasion PMID: 28698064 Proto-oncogene proteins c-met (MET) mutations Y1248H and D1246N confer resistance in vitro and in vivo. PMID: 28396313 MET overexpression is found in 23.8% of surgically resected NSCLC. MET amplification prevails in 4.6% and is associated with MET overexpression. Both have no influence on prognosis. PMID: 28838386 study highlights the role of tissue differentiation on pathological response to neoadjuvant chemotherapy in gastric cancer and shows no impact between FOXP3, HER2 and MET expression in terms of tumor regression grading PMID: 29696715 Show More Hide All
Involvement in disease	Hepatocellular carcinoma (HCC); Renal cell carcinoma papillary (RCCP); Deafness, autosomal recessive, 97 (DFNB97); Osteofibrous dysplasia (OSFD)
Subcellular Location	Membrane, Single-pass type I membrane protein, SUBCELLULAR LOCATION: Isoform 3: Secreted
Protein Families	Protein kinase superfamily, Tyr protein kinase family
Tissue Specificity	Expressed in normal hepatocytes as well as in epithelial cells lining the stomach, the small and the large intestine. Found also in basal keratinocytes of esophagus and skin. High levels are found in liver, gastrointestinal tract, thyroid and kidney. Also
Database Links	HGNC: 7029 OMIM: 114550 KEGG: hsa:4233 STRING: 9606.ENSP00000317272 UniGene: Hs.132966

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Code	CSB-MP013714HU
Size	$298Purchase it in Cusabio online store (only available for customers from the US)
Image	(Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel. Activity Measured by its binding ability in a functional ELISA. Immobilized MET at 2 μg/ml can bind Anti-MET recombinant antibody, the EC₅₀ is 2.379-3.094 ng/ml. Biological Activity Assay
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Recombinant Human Hepatocyte growth factor receptor(MET),partial (Active)

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