抗HGF Receptor抗体(Anti-HGF Receptor, Mouse-Mono, FITC antibody)

• 価格
• Product Details
• Applications and Data
• Related Product & Information
• Citations

価格

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Product Details

Species Reactivity	Human
Label	Fluorescein
Immunogen	Mouse myeloma cell line NS0-derived recombinant human HGF R/c-METGlu25-Thr932Accession # P08581
Source	Monoclonal Mouse IgG1 Clone # 95106
Purification	Protein A or G purified from hybridoma culture supernatant
Specificity	Detects human HGF R/c-MET.

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Applications and Data

	Recommended Concentration	Sample
Flow Cytometry	10 µL/106 cells	See below

Flow Cytometry
	Detection of HGF R/c‑MET in MDA‑MB‑231 Human Cell Line by Flow Cytometry. MDA‑MB‑231 human breast cancer cell line was stained with Mouse Anti-Human HGF R/c‑MET Fluorescein‑conjugated Monoclonal Antibody (Catalog # FAB3582F, filled histogram) or isotype control antibody (Catalog # IC002F, open histogram). View our protocol for Staining Membrane-associated Proteins.

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Related Product & Information

Background

HGF R/c-MET

background_content

Background: HGF R/c-MET HGF R, also known as Met (from N-methyl-N’-nitro-N-nitrosoguanidine induced), is a glycosylated receptor tyrosine kinase that plays a central role in epithelial morphogenesis and cancer development. HGF R is synthesized as a single chain precursor which undergoes cotranslational proteolytic cleavage. This generates a mature HGF R that is a disulfide-linked dimer composed of a 50 kDa extracellular alpha chain and a 145 kDa transmembrane beta chain (1, 2). The extracellular domain (ECD) contains a seven bladed beta -propeller sema domain, a cysteine-rich PSI/MRS, and four Ig-like E-set domains, while the cytoplasmic region includes the tyrosine kinase domain (3, 4). Proteolysis and alternate splicing generate additional forms of human HGF R which either lack of the kinase domain, consist of secreted extracellular domains, or are deficient in proteolytic separation of the alpha and beta chains (5-7). The sema domain, which is formed by both the alpha and beta chains of HGF R, mediates both ligand binding and receptor dimerization (3, 8). Ligand-induced tyrosine phosphorylation in the cytoplasmic region activates the kinase domain and provides docking sites for multiple SH2-containing molecules (9, 10). HGF stimulation induces HGF R downregulation via internalization and proteasome-dependent degradation (11). In the absence of ligand, HGF R forms non-covalent complexes with a variety of membrane proteins including CD44v6, CD151, EGF R, Fas, Integrin alpha 6/ beta 4, Plexins B1, 2, 3, and MSP R/Ron (12-19). Ligation of one complex component triggers activation of the other, followed by cooperative signaling effects (12-19). Formation of some of these heteromeric complexes is a requirement for epithelial cell morphogenesis and tumor cell invasion (12, 16, 17). Paracrine induction of epithelial cell scattering and branching tubulogenesis results from the stimulation of HGF R on undifferentiated epithelium by HGF released from neighboring mesenchymal cells (20). Genetic polymorphisms, chromosomal translocation, over-expression, and additional splicing and proteolytic cleavage of HGF R have been described in a wide range of cancers (1). Within the ECD, human HGF R shares 86-88% amino acid sequence identity with canine, mouse, and rat HGF R.

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Citations

1. Growth-factor-driven rescue to receptor tyrosine kinase (RTK) inhibitors through Akt and Erk phosphorylation in pediatric low grade astrocytoma and ependymoma.
   Authors: Sie M, den Dunnen W, Lourens H, Meeuwsen-de Boer T, Scherpen F, Zomerman W, Kampen K, Hoving E, de Bont E
   PLoS ONE, 2015;10(3):e0122555.
   Species: Human
   Sample Type: Whole Cells
   Application: Flow


2. CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.
   Authors: Todaro M, Gaggianesi M, Catalano V, Benfante A, Iovino F, Biffoni M, Apuzzo T, Sperduti I, Volpe S, Cocorullo G, Gulotta G, Dieli F, De Maria R, Stassi G
   Cell Stem Cell, 2014;14(3):342-56.
   Species: Human
   Sample Type: Whole Cells
   Application: Flow


3. Activated platelets interfere with recruitment of mesenchymal stem cells to apoptotic cardiac cells via high mobility group box 1/Toll-like receptor 4-mediated down-regulation of hepatocyte growth factor receptor MET.
   Authors: Vogel S, Chatterjee M, Metzger K, Borst O, Geisler T, Seizer P, Muller I, Mack A, Schumann S, Buhring H, Lang F, Sorg R, Langer H, Gawaz M
   J Biol Chem, 2014;289(16):11068-82.
   Species: Human
   Sample Type: Whole Cells
   Application: Flow

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