Human Recombinant MET protein, ECD, AF647 Conjugated, His Tag (V2LY-0526-LY3250)

Name: Human Recombinant MET protein, ECD, AF647 Conjugated, His Tag
SKU: V2LY-0526-LY3250
Rating: 5 (1 reviews)

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Datasheet

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Expressed Host

HEK293 Cells

Protein Species

Human

Tag

His Tag

Protein Construction

This product is Human Recombinant MET protein, ECD, AF647 Conjugated, His Tag consist of Amino Acid: 1-932 and predicts a molecular mass of 105.1 kDa.

Molecule Mass

105.1 kDa

Protein Domain

ECD

Conjugates

AF647

Sequence

Amino Acid: 1-932

Species

Human

Formulations & Storage [For reference only, actual COA shall prevail!]

Endotoxin

Please contact us for more information.

Format

Lyophilized

Reconstitution

Allow the vial and reconstitution buffer to equilibrate to room temperature. Briefly centrifuge or tap down the vial to ensure that all lyophilized powder is collected at the bottom of the vial. For the reconstitution of this product, we recommend adding PBS or sterile water to achieve a final antibody concentration of 1 mg/mL. Allow the vial to reconstitute for 10-15 minutes at room temperature with gentle agitation. Avoid vigorous shaking that can cause foaming and antibody denaturation. Aliquot into volumes based on your experiment and store liquid protein at -20°C or -80°C for long time.

Buffer

Lyophilized from sterile PBS

Preservative

None

Storage

Twelve months from date of receipt at -20°C to -70°C in lyophilized form and 3 months at -70°C under sterile conditions after reconstitution. Protect from prolonged exposure to light and avoid repeated freeze-thaw cycles.

More Infomation

Target

Full Name

MET Proto-Oncogene, Receptor Tyrosine Kinase

Function

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).

(Microbial infection) Acts as a receptor for Listeria monocytogenes internalin InlB, mediating entry of the pathogen into cells.

Biological Process

Branching morphogenesis of an epithelial tube Source: UniProtKB
Cell migration Source: GO_Central
Cell surface receptor signaling pathway Source: UniProtKB
Endothelial cell morphogenesis Source: UniProtKB
Entry of bacterium into host cell Source: Reactome
Establishment of skin barrier Source: CAFA
Liver development Source: GO_Central
MAPK cascade Source: Reactome
Multicellular organism development Source: GO_Central
Negative regulation of autophagy Source: ParkinsonsUK-UCL
Negative regulation of guanyl-nucleotide exchange factor activity Source: CAFA
Negative regulation of hydrogen peroxide-mediated programmed cell death Source: BHF-UCL
Negative regulation of Rho protein signal transduction Source: CAFA
Negative regulation of stress fiber assembly Source: CAFA
Negative regulation of thrombin-activated receptor signaling pathway Source: CAFA
Nervous system development Source: GO_Central
Neuron differentiation Source: GO_Central
Pancreas development Source: GO_Central
Phagocytosis Source: GO_Central
Positive chemotaxis Source: UniProtKB
Positive regulation of endothelial cell chemotaxis Source: UniProtKB
Positive regulation of kinase activity Source: GO_Central
Positive regulation of microtubule polymerization Source: CAFA
Positive regulation of protein kinase B signaling Source: GO_Central
Positive regulation of transcription by RNA polymerase II Source: BHF-UCL
Semaphorin-plexin signaling pathway Source: UniProtKB
Signal transduction Source: ProtInc
Transmembrane receptor protein tyrosine kinase signaling pathway Source: GO_Central

Cellular Location

Membrane
Isoform 3: Secreted

Involvement in disease

Activation of MET after rearrangement with the TPR gene produces an oncogenic protein.
Defects in MET may be associated with gastric cancer.
Hepatocellular carcinoma (HCC):
A primary malignant neoplasm of epithelial liver cells. The major risk factors for HCC are chronic hepatitis B virus (HBV) infection, chronic hepatitis C virus (HCV) infection, prolonged dietary aflatoxin exposure, alcoholic cirrhosis, and cirrhosis due to other causes.
Renal cell carcinoma papillary (RCCP):
A subtype of renal cell carcinoma tending to show a tubulo-papillary architecture formed by numerous, irregular, finger-like projections of connective tissue. Renal cell carcinoma is a heterogeneous group of sporadic or hereditary carcinoma derived from cells of the proximal renal tubular epithelium.
A common allele in the promoter region of the MET shows genetic association with susceptibility to autism in some families. Functional assays indicate a decrease in MET promoter activity and altered binding of specific transcription factor complexes.
MET activating mutations may be involved in the development of a highly malignant, metastatic syndrome known as cancer of unknown primary origin (CUP) or primary occult malignancy. Systemic neoplastic spread is generally a late event in cancer progression. However, in some instances, distant dissemination arises at a very early stage, so that metastases reach clinical relevance before primary lesions. Sometimes, the primary lesions cannot be identified in spite of the progresses in the diagnosis of malignancies.
Deafness, autosomal recessive, 97 (DFNB97):
A form of non-syndromic sensorineural hearing loss with prelingual onset. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information.
Osteofibrous dysplasia (OSFD):
Disease susceptibility is associated with variants affecting the gene represented in this entry. Disease-associated variants identified in 4 families cause the deletion of exon 14. This results in the exclusion of an ubiquitination target site within the cytoplasmic domain, hence in protein stabilization. The persistent presence of MET at the cell surface in conditions of ligand-dependent activation retards osteoblastic differentiation.
A congenital disorder of osteogenesis characterized by non-neoplastic, radiolucent lesions that affect the cortical bone immediately under the periosteum. It usually manifests as a painless swelling or anterior bowing of the long bones, most commonly the tibia and fibula.

Topology

Extracellular: 25-932
Helical: 933-955
Cytoplasmic: 956-1390

PTM

Autophosphorylated in response to ligand binding on Tyr-1234 and Tyr-1235 in the kinase domain leading to further phosphorylation of Tyr-1349 and Tyr-1356 in the C-terminal multifunctional docking site. Dephosphorylated by PTPRJ at Tyr-1349 and Tyr-1365. Dephosphorylated by PTPN1 and PTPN2.
Ubiquitinated. Ubiquitination by CBL regulates MET endocytosis, resulting in decreasing plasma membrane receptor abundance, and in endosomal degradation and/or recycling of internalized receptors.
(Microbial infection) Tyrosine phosphorylation is stimulated by L.monocytogenes InlB. Tyrosine phosphorylation is maximal 10-20 minutes after treatment with InlB and disappears by 60 minutes. The phosphorylated residues were not identified.

Yao, Y., Yang, H., Zhu, B., Wang, S., Pang, J., Wu, X., ... & Zhao, Z. (2023). Mutations in the MET tyrosine kinase domain and resistance to tyrosine kinase inhibitors in non-small-cell lung cancer. Respiratory Research, 24(1), 28.

Fernandes, M., Jamme, P., Cortot, A. B., Kherrouche, Z., & Tulasne, D. (2021). When the MET receptor kicks in to resist targeted therapies. Oncogene, 40(24), 4061-4078.

Coleman, N., Hong, L., Zhang, J., Heymach, J., Hong, D., & Le, X. (2021). Beyond epidermal growth factor receptor: MET amplification as a general resistance driver to targeted therapy in oncogene-driven non-small-cell lung cancer. ESMO open, 6(6), 100319.

Malik, R., Mambetsariev, I., Fricke, J., Chawla, N., Nam, A., Pharaon, R., & Salgia, R. (2020). MET receptor in oncology: from biomarker to therapeutic target. Advances in cancer research, 147, 259-301.

Weng, T. H., Yao, M. Y., Xu, X. M., Hu, C. Y., Yao, S. H., Liu, Y. Z., ... & Yao, H. P. (2020). RON and MET co-overexpression are significant pathological characteristics of poor survival and therapeutic targets of tyrosine kinase inhibitors in triple-negative breast cancer. Cancer Research and Treatment: Official Journal of Korean Cancer Association, 52(3), 973-986.

Hu, C. Y., Xu, X. M., Hong, B., Wu, Z. G., Qian, Y., Weng, T. H., ... & Yao, H. P. (2019). Aberrant RON and MET co-overexpression as novel prognostic biomarkers of shortened patient survival and therapeutic targets of tyrosine kinase inhibitors in pancreatic cancer. Frontiers in Oncology, 9, 1377.

Fernandes, M., Duplaquet, L., & Tulasne, D. (2019). Proteolytic cleavages of MET: the divide-and-conquer strategy of a receptor tyrosine kinase. BMB reports, 52(4), 239.

Orlando, E., Aebersold, D. M., Medova, M., & Zimmer, Y. (2019). Oncogene addiction as a foundation of targeted cancer therapy: The paradigm of the MET receptor tyrosine kinase. Cancer letters, 443, 189-202.

Guo, R., Berry, L. D., Aisner, D. L., Sheren, J., Boyle, T., Bunn Jr, P. A., ... & Kris, M. G. (2019). MET IHC is a poor screen for MET amplification or MET exon 14 mutations in lung adenocarcinomas: data from a tri-institutional cohort of the lung cancer mutation consortium. Journal of Thoracic Oncology, 14(9), 1666-1671.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

Alternative Versions

Rabbit Anti-MET (Phosphorylated Y1003) Recombinant Antibody (CAT#: PTM-CBMAB-0974LY)

Canine Recombinant MET protein, His Tag (CAT#: V2LY-0526-LY1227)

Cynomolgus, Rhesus Recombinant MET protein (CAT#: V2LY-0526-LY1697)

Cynomolgus, Rhesus Recombinant MET protein, hFc Tag (CAT#: V2LY-0526-LY1698)

Cynomolgus, Rhesus Recombinant MET protein, Biotin Conjugated, His Tag (CAT#: V2LY-0526-LY1699)

Cynomolgus, Rhesus Recombinant MET protein, His Tag (CAT#: V2LY-0526-LY1700)

Cynomolgus, Rhesus Recombinant MET protein, His Tag-1 (CAT#: V2LY-0526-LY1701)

Human Recombinant MET protein, GST Tag (CAT#: V2LY-0526-LY3249)

Human Recombinant MET protein, APC Conjugated, His Tag (CAT#: V2LY-0526-LY3251)

Human Recombinant MET (D1213H), Active protein, GST Tag (CAT#: V2LY-0526-LY3252)

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For research use only. Not intended for any clinical use.

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