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HAF017). Specific bands were detected for HGF R/c-MET at approximately 150-200 kDa (as indicated) in the parental HeLa cell line, but is not detectable in knockout HeLa cell line. GAPDH (AF5718) is shown as a loading control. This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1." class="big_lightbox" target="_blank">
AB-108-C, open histogram) followed by Phycoerythrin-conjugated Anti-Goat IgG Secondary Antibody (Catalog # F0107). View our protocol for Staining Membrane-associated Proteins." class="big_lightbox" target="_blank">
358-MT) was serially diluted and captured by Mouse Anti-Human HGFR/c-MET Monoclonal Antibody (Catalog # MAB3581) coated on a Clear Polystyrene Microplate (Catalog # DY990). Goat Anti-Human HGFR/c-MET Antigen Affinity-purified Polyclonal Antibody (Catalog # AF276) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998)" class="big_lightbox" target="_blank">
CTS008) and counterstained with hematoxylin (blue). Specific staining was localized to cytoplasm in muscle cells. View our protocol for Chromogenic IHC Staining of Frozen Tissue Sections." class="big_lightbox" target="_blank">
527-ME) was serially diluted and captured by Rat Anti-Mouse HGFR/c-MET Monoclonal Antibody (Catalog # MAB5271) coated on a Clear Polystyrene Microplate (Catalog # DY990). Goat Anti-Mouse HGFR/c-MET Antigen Affinity-purified Polyclonal Antibody (Catalog # AF527) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998)" class="big_lightbox" target="_blank">
AF276) immunoprecipitate of MDA-MB-468 human breast cancer cell line untreated (-) or treated (+) with 100 µM pervanadate (PV) for 10 minutes. PVDF membrane was probed with 0.5 µg/mL of Rabbit Anti-Human/Mouse Phospho-HGF R/c-MET (Y1234/Y1235) Antigen Affinity-purified Polyclonal Antibody (Catalog # AF2480), followed by HRP-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # HAF008). A specific band was detected for Phospho-HGF R/c-MET (Y1234/Y1235) at approximately 145 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1." class="big_lightbox" target="_blank">
VC003). Before incubation with the primary antibody, tissue was subjected to heat-induced epitope retrieval using Antigen Retrieval Reagent-Basic (Catalog # CTS013). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to cytoplasm. View our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents." class="big_lightbox" target="_blank">
AB-105-C, blue open histogram), followed by Phycoerythrin-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # F0110). To facilitate intracellular staining, cells were fixed with paraformaldehyde and permeabilized with methanol." class="big_lightbox" target="_blank">
BAM1676) to detect phospho-HGF R (p-HGF R). Bands were visualized with Streptavidin-HRP (Cat # DY998) followed by chemiluminescent detection using WesternGloTM Chemiluminescent Detection Substrate (Catalog # AR004)." class="big_lightbox" target="_blank">
358-MT), human EGF R (Catalog #1095-ER) or human IGF-I sR (Catalog #305-GR) were added to 50 μg lysate and analyzed using this ELISA. Competition was observed only with recombinant HGF R. " class="big_lightbox" target="_blank">
Met is a receptor protein-tyrosine kinase (RPTK) for hepatocyte growth factor (HGF), which is a multifunctional cytokine controlling cell growth, morphogenesis, and motility. Met overexpression has been identified in a variety of human cancers (1). Met kinase domain possesses unique features that distinguish met from other members of the src family of protein tyrosine kinases. These results also demonstrate that the product of the activated met gene is a fusion protein and that the amino terminal end of this fusion protein exhibits homology to laminin B1 (2). Data suggest that RanBP9, functioning as an adaptor protein for the Met tyrosine kinase domain, can augment the HGF-Met signaling pathway and that RanBP9 overexpression may cause constitutive activation of the Ras signaling pathway (1). Hereditary papillary renal carcinoma (HPRC) is a recently recognized form of inherited kidney cancer Results suggest that missense mutations located in the MET proto-oncogene lead to constitutive activation of the Met protein and papillary renal carcinomas (3)