44-888G

antibody from Invitrogen Antibodies

Targeting: MET DFNB97, HGFR, RCCP2

Provider product page for 44-888G

Western blot

ELISA

Other assay

Antibody data

Antibody Data
Antigen structure
References [34]
Comments [0]
Validations
Western blot [1]
Other assay [16]

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Product number: 44-888G - Provider product page
Provider: Invitrogen Antibodies
Product name: Phospho-c-Met (Tyr1230, Tyr1234, Tyr1235) Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Reactivity: Human, Mouse
Host: Rabbit
Isotype: IgG
Vial size: 100 µL
Storage: -20°C

MET protein structure - 44-888G shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: c-Met (pYpYpY1230/1234/1235) ELISA Peptide Blocking.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 5 VEGF 165 induces c-MET activation through a NRP1-dependent mechanism . (a) Effects of NRP1 depletion on VEGF 165 -mediated c-MET phosphorylation. ARCaP M cells were transfected with NRP1 siRNA or control siRNA for 48 h, serum-starved overnight, then treated with VEGF 165 (10 ng/ml) for 60 min. (b) Immunoprecipitation assay of NRP1-c-MET interaction. Serum-starved ARCaP M cells were treated with VEGF 165 (10 ng/ml) for the indicated times, and immunoprecipitated with anti-NRP1 (upper), or anti-c-MET (low) antibody. (c) Co-localization of NRP1 and c-MET or p-c-MET. Serum-starved ARCaP M cells were treated with VEGF 165 (10 ng/ml) or PBS for the indicated times. Immunofluorescence staining of NRP1, c-MET or p-c-MET was performed and visualized by confocal microscopy. Arrows indicate co-localization of NRP1 and c-MET or p-c-MET.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 8 Expression of NRP1 and p-c-MET is associated with bone metastatic status of human PCa specimens and the ARCaP M model . IHC analyses of NRP1 expression in human normal/benign, cancerous and metastatic prostatic tissue specimens (a) and primary and bone metastatic tissue specimens from ARCaP M model (b), and of p-c-MET expression in human PCa progression (c) and ARCaP M xenografts (d). Arrows indicate positively-stained cells.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 2 RANKL overexpression activated c-Met signaling components detected by single quantum dot labeling, SQDL. Differential QD labeling of proteins was performed in LNCaP-neo ( A ) and LNCaP-RANKL ( B ) cells using DAPI nuclear staining as reference. For each analysis, QD labeled protein expression is presented in pseudocolor, with the overlaid image of DAPI and QD signals (Merged). x400.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 5 Multiplexed quantum dot labeling (MQDL) simultaneously detected c-Met activated and EMT genes in a CRPC LTL-313 xenograft model. Single tumor tissue sections from intact and castrated hosts were subjected to sequential MQDL. Enhanced expression of c-Met activated genes was detected in tumor tissues from castrated hosts. ( A ) A stack of multiple images (Cube), nuclear staining (DAPI), and individual gene expression (in pseudocolors) are shown. Gene expression signals were superimposed with DAPI nuclear signals to yield a composite image for analysis. x400. ( B ) Significant differences in gene expression were found by quantification analysis of 1,000 cells in each tumor specimen using inForm software ( P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 4 Castration induced c-Met activated and EMT associated proteins. The c-Met activated and EMT associated proteins were detected in the CRPC LTL-313 xenograft model by conventional IHC (A) and SQDL (B). Castration increased a panel of genes in LTL-313 xenograft prostate cancer and decreased AR expression compared to xenografts obtained from intact hosts by both IHC and SQDL. x400.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1 RANKL overexpression induced epithelial to mesencymal transition. RANKL-transfected LNCaP cells induced EMT in histomorphology (A) and gene expression in mRNA (B) and protein (C). Data represent one of 3 RANKL-stably transfected and 2 neo-stably transfected LNCaP cell clones.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 MiR-199a-3p inhibits cell proliferation, adhesion and invasion through the suppression of c-Met expression (A) Western blotting. SKOV3ip1 cells were transfected with pre-miR-199a-3p or negative control miR for 24 hours. Cell lysate were collected before and after HGF stimulation (40 ng/mL, 10 minutes). Immunoblotting was performed with antibodies against phosphorylated c-Met (p-c-Met), c-Met, phosphorylated extracellular signal-regulated kinase (p-ERK), phosphorylated Akt (p-Akt), or beta-actin. (B) Colony formation assay. Ovarian cancer cells (1 x 10 5 cells; SKOV3ip1 and RMUG-S), cotransfected with miRNA (pre-miR-199a-3p or negative control miRNA) and an pIRES2-EGFP vector (containing MET or the empty control vector), were suspended in 0.33% agarose. After 10 days, colonies with a diameter greater than 100 mum were counted under a microscope at 40x magnification. Representative images are shown. Bar represents 400 mum. Data represent mean +- SEM; n = 10. (C) In vitro adhesion assay. SKOV3ip1 (5 x 10 4 ) cells were cotransfected with miRNA (pre-miR-199a-3p or negative control miR) and the pIRES2-EGFP vector (containing MET or the empty control vector). The cells were plated onto 50 mug/mL fibronectin- or collagen type 1-coated 96-well plates. After being incubated for 75 minutes at 37degC, the plates were washed to discard nonadherent cells, and the number of adherent cells was counted. Representative images are shown. Bar represents 100 mum. Data represent mean +-

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 Cellular effects of siRNA-mediated MET -specific gene knock-down in HNSCC cell lines. ( A ) Validation of down-regulated c-MET protein expression 24 h upon transfection with 50 pmol of c-MET specific siRNA#1 and #2 in comparison to unspecific scrambled control (scr). Western blot analysis demonstrated highly efficient c-MET (175 kDa) down-regulation in Cal33 and FaDu as well as their irradiated sublines (IR). Glyceraldehyde 3-phosphate dehydrogenase (GAPDH, 35 kDa) was used as internal loading control ( n = 2). ( B,C ) Clonogenic survival and plating efficiency (b) in standard 2D-colony-assay 10 days after c-MET knock-down for Cal33 and FaDu cell line as well as their irradiated sub-lines (IR) in comparison to scramble (scr) control ( n = 3, * p < 0.05, mean +- SEM). Linear-quadratic model of cell survival curves after irradiation with 0, 2, 4, or 6 Gy (c) ( n = 3, * p < 0.05, mean +- SEM). The number of colonies within 10 days is calculated to plated cell number and depicted as plating efficiency. The surviving fraction illustrates the clonogenic survival depending on the irradiation dose and is normalized to plating efficiency. ( D ) Western blot analysis of Detroit562 cells 24 h after c-MET knock-down validated the effects on c-MET proteins without affecting c-MET phosphorylation and other downstream kinases such as AKT and ERK1/2. beta-actin was used as loading control. ( E ) Clonogenic survival of metastasis cell line Detroit562 which originates from pleural eff