MET (Ab-1003) Antibody

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Product Specs

Form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Lead Time
Typically, we can ship the products within 1-3 business days after receiving your order. Delivery time may vary depending on the purchasing method or location. Please consult your local distributors for specific delivery time information.
Synonyms
AUTS9 antibody; c met antibody; D249 antibody; Hepatocyte growth factor receptor antibody; HGF antibody; HGF receptor antibody; HGF/SF receptor antibody; HGFR antibody; MET antibody; Met proto oncogene antibody; Met proto oncogene tyrosine kinase antibody; MET proto oncogene; receptor tyrosine kinase antibody; Met proto-oncogene (hepatocyte growth factor receptor) antibody; Met proto-oncogene antibody; Met protooncogene antibody; MET_HUMAN antibody; Oncogene MET antibody; Par4 antibody; Proto-oncogene c-Met antibody; RCCP2 antibody; Scatter factor receptor antibody; SF receptor antibody; Tyrosine-protein kinase Met antibody
Target Names
MET
Uniprot No.

Target Background

Function
MET is a receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. It plays a crucial role in regulating various physiological processes including proliferation, scattering, morphogenesis, and survival. Upon ligand binding at the cell surface, MET undergoes autophosphorylation on its intracellular domain, creating docking sites for downstream signaling molecules. Following activation by ligand, MET interacts with PIK3R1, PLCG1, SRC, GRB2, STAT3, or the adapter GAB1, components of the PI3-kinase subunit. The 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 pathways. The RAS-ERK activation is associated with morphogenetic effects, while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling is essential for gastrulation, development and migration of muscles and neuronal precursors, angiogenesis, and kidney formation. In adults, MET participates in wound healing, organ regeneration, and tissue remodeling. Additionally, it promotes differentiation and proliferation of hematopoietic cells and may regulate cortical bone osteogenesis. Notably, MET acts as a receptor for Listeria monocytogenes internalin InlB, facilitating the entry of this pathogen into cells.
Gene References Into Functions
  1. The miR-19a/c-Met pathway is crucial in acquired resistance to gefitinib. Manipulating miR-19a might offer a therapeutic approach to overcome acquired gefitinib resistance. PMID: 28592790
  2. The expression of C-Met and HER2 proteins in lung adenocarcinoma is highly correlated. Further investigation is needed to determine if their combined presence has synergistic effects in the targeted therapy of lung adenocarcinoma. PMID: 29400000
  3. MET overexpression is more prevalent in high-grade myxofibrosarcoma and the epithelioid variant. Chromosome 7 polysomy, rather than MET gene regional amplification, may contribute to the overexpression of MET protein. PMID: 30126419
  4. miR-449a suppresses hepatocellular carcinoma tumorigenesis by downregulating activity in the c-Met/ERK pathway. PMID: 30108016
  5. MET amplifications have been identified in two cases of endometrial clear-cell carcinoma with mixed features. PMID: 29633423
  6. NGS enables the detection of low-abundant ctDNA in blood based on ultra-deep sequencing. This technology facilitated the identification of MET exon 14 skipping in a patient who responded to crizotinib despite the low abundance of the mutation. This case highlights the feasibility of choosing targeted therapy even with low abundance of gene mutations. PMID: 29110851
  7. The interplay of dual MET/HER2 overexpression in the AKT and ERK pathways for esophageal cancer is described. This suggests that combination therapy could be a novel strategy for esophageal adenocarcinoma (EAC) with amplification of both MET and HER2. PMID: 29223420
  8. 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
  9. MET Exon 14 Skipping Mutations in Non-small Cell Lung Cancer PMID: 30037377
  10. MET activation, either by METex14 mutations or amplification, is characteristic of a subset of early stage NSCLCs and may coexist with ERBB2 amplification. PMID: 29139039
  11. Serum levels of miR-658 are significantly lower in the NM group than in the DM group. Concurrently, the levels of PAX3 and MET are also lower in the NM group than in the DM group. Both overexpression and silencing of miR-658 significantly upregulate or downregulate the levels of PAX3 and MET in gastric cell lines. PMID: 29630524
  12. MiR-206 inhibits the development of epithelial ovarian cancer cells by directly targeting c-Met and inhibiting the c-Met/AKT/mTOR signaling pathway. PMID: 29807226
  13. Gastric cancer progression is not associated with a unique signaling pathway. A feedback loop may exist between the HGF/c-Met and Notch1 signaling pathways, potentially leading to therapeutic resistance. PMID: 29781036
  14. Comparative analysis revealed a strong association between MET expression and MET amplification (85% concurrence) in primary stomach tumors and matched liver metastasis. Survival analyses indicate that both MET amplification and MET overexpression are prognostic of poor outcomes. PMID: 29790169
  15. High c-met expression is associated with oral squamous cell carcinoma. PMID: 29286169
  16. FOXO1 acts as a critical regulator of the acquired lapatinib resistance in HER2-positive GC cells. It serves as a crucial link between HER2 and MET signaling pathways through negative crosstalks. PMID: 28343375
  17. This research explores the potential of cMET blockade in augmenting radiation therapy for patients with NF2. PMID: 29440379
  18. This study highlights the significance of cross-species protein interactions between murine feeder cells and human epithelial cells in 3T3-J2 co-culture. It demonstrates that STAT6 phosphorylation occurs in response to MET activation in epithelial cells. However, STAT6 nuclear translocation does not occur in response to HGF, preventing the transcriptional activity of STAT6. PMID: 29771943
  19. c-Met-activated Mesenchymal Stem Cells (MSC) pre-exposed to hypoxia interact with PrPC at the site of ischemic injury, enhancing the efficiency of MSC transplantation. PMID: 29705776
  20. A novel G-quadruplex motif has been identified within the Human MET promoter region. PMID: 29054971
  21. A METex14 del mutation-positive NSCLC patient who responded to crizotinib but later relapsed, demonstrated a mixed response to glesatinib. This included reduction in size of a MET Y1230H mutation-positive liver metastasis and concurrent loss of detection of this mutation in plasma DNA. These findings suggest that glesatinib exhibits a distinct mechanism of target inhibition and can overcome resistance to PMID: 28765324
  22. This study demonstrates that simultaneous inhibition of c-Met and Src signaling in MD-MSCs triggers apoptosis, revealing vulnerable pathways that could be exploited for the development of NF2 therapies. PMID: 28775147
  23. Prolonged treatment with single HGF/c-Met or Hh inhibitors can lead to resistance. This is likely due to enhanced expression of Shh following c-Met treatment, and vice versa. Targeting both the HGF/c-Met and Hh pathways simultaneously overcomes resistance to single-inhibitor treatment and leads to a more potent antitumor effect in combination with chemotherapy. PMID: 28864680
  24. This study identifies 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
  25. TGF-beta negatively controls the HGF/c-MET pathway by regulating stemness in glioblastoma. PMID: 29238047
  26. Preclinical efficacy and safety data provide a strong rationale for ongoing clinical studies of Sym015 in patients with MET-amplified tumors. PMID: 28679766
  27. High MET expression is associated with malignant pleural mesothelioma. PMID: 28560410
  28. 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 involve the inhibition of the NF-kappaB pathway and c-Met expression. PMID: 29039556
  29. c-Met expression is significantly increased in human oral squamous cell carcinoma (OSCC) tissues compared to normal mucosa adjacent to the tumor, but it is not correlated with clinicopathological parameters. These findings suggest a potential role of c-Met in the progression of OSCC. PMID: 29115556
  30. S49076 exhibits cytotoxic activity at low doses on MET-dependent cells through MET inhibition. It inhibits the growth of MET-independent cells at higher but clinically relevant doses by targeting Aurora B. PMID: 28619752
  31. MET expression is significantly reduced in the superior temporal gyrus cortex of individuals with autism spectrum disorders. PMID: 28322981
  32. In squamous cell carcinoma of the head and neck (SCCHN), immunohistochemical overexpression of c-MET above cut-off levels III and particularly II is associated with inferior survival outcomes and advanced disease. PMID: 29103754
  33. Three patients with cMET amplification achieved partial response on Crizotinib. PMID: 29199685
  34. The c-Met/beta1 integrin complex, whose ligand-independent cross-activation and robust affinity for fibronectin drive invasive oncologic processes. PMID: 28973887
  35. 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
  36. MET mutations have been found in cancer of unknown primary origin (CUP), clustered to the SEMA and TK domain of the receptor. The biomechanical properties of MET mutants might trigger the hyper-invasive phenotype associated with CUP. [review] PMID: 29037604
  37. 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
  38. 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
  39. EGFR mutation is 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
  40. Oncogene E5 is primarily responsible for Met upregulation. E5-induced Met contributes to the motility of HPV-containing cells. These studies highlight a new role for E5 in epithelial-stromal interactions, with implications for cancer development. PMID: 29609071
  41. EGFR T790M mutation and cMET amplification are main mechanisms leading to EGFR TKI resistance in lung adenocarcinoma. PMID: 29616327
  42. MET activation is associated with drug resistance in chronic myeloid leukemia. PMID: 28418880
  43. High glucose activates Met receptor in HK2 cells independently of HGF, via induction of integrin a5b1 and downstream signaling. This mode of Met activation is associated with tubular cell damage and apoptosis and may represent a novel pathogenic mechanism and a treatment target in diabetic nephropathy. PMID: 28819999
  44. This study explores gene copy number (GCN) variation of EGFR, HER2, c-MYC, and MET in patients with primary colorectal cancer. PMID: 28764718
  45. The HGF/c-MET pathway mediates VEGFR inhibitor resistance and vascular remodeling in NSCLC. PMID: 28559461
  46. Because c-Met is strongly associated with pathological grade, stage, and disease-specific survival, c-Met levels may have the potential to predict patient prognosis and to guide clinical diagnosis and treatment of patients with renal cell carcinoma. PMID: 28427859
  47. 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
  48. Proto-oncogene proteins c-met (MET) mutations Y1248H and D1246N confer resistance in vitro and in vivo. PMID: 28396313
  49. MET overexpression is found in 23.8% of surgically resected NSCLC. MET amplification prevails in 4.6% and is associated with MET overexpression. Neither factor significantly influences prognosis. PMID: 28838386
  50. This study highlights the role of tissue differentiation on pathological response to neoadjuvant chemotherapy in gastric cancer. It shows no impact between FOXP3, HER2, and MET expression in terms of tumor regression grading. PMID: 29696715

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Database Links

HGNC: 7029

OMIM: 114550

KEGG: hsa:4233

STRING: 9606.ENSP00000317272

UniGene: Hs.132966

Involvement In Disease
Hepatocellular carcinoma (HCC); Renal cell carcinoma papillary (RCCP); Deafness, autosomal recessive, 97 (DFNB97); Osteofibrous dysplasia (OSFD)
Protein Families
Protein kinase superfamily, Tyr protein kinase family
Subcellular Location
Membrane; Single-pass type I membrane protein.; [Isoform 3]: Secreted.
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

Q&A

What is MET (Ab-1003) Antibody and what epitope does it recognize?

MET (Ab-1003) Antibody is a rabbit polyclonal antibody that specifically detects endogenous levels of total MET protein. It recognizes a peptide sequence around amino acids 1001-1005 (V-D-Y-R-A) derived from Human MET . This antibody binds to the MET protein, also known as hepatocyte growth factor receptor (HGFR) or c-Met, which plays crucial roles in cell growth, survival, and migration.

What applications has this antibody been validated for?

The antibody has been validated for Western Blot (WB) and Immunohistochemistry (IHC) applications primarily . Some sources also indicate it may be suitable for Immunofluorescence (IF) and ELISA . Published research demonstrates its successful application in detecting MET in human tissue samples and cell lines such as HepG2 and A549 .

What species reactivity does MET (Ab-1003) Antibody demonstrate?

The antibody shows consistent reactivity with Human, Mouse, and Rat samples , making it versatile for comparative studies across these species. This cross-species reactivity is particularly valuable for translational research between animal models and human samples.

What is the recommended dilution range for different applications?

The optimal dilution ranges are:

  • Western Blot (WB): 1:500 to 1:3000

  • Immunohistochemistry (IHC-P): 1:50 to 1:100

  • Immunofluorescence (IF): 1:100 to 1:500

Researchers should perform titration experiments in their specific experimental systems to determine optimal working concentrations.

What positive and negative controls should be used with MET (Ab-1003) Antibody?

For positive controls, HepG2 cells have been validated and show strong MET expression when detected with this antibody . A549 cells are also suitable for immunofluorescence applications . For negative controls, consider:

  • Secondary antibody-only controls

  • Peptide competition assays using the immunogenic peptide

  • Tissues or cell lines with knocked-down MET expression

How should MET (Ab-1003) Antibody be stored and handled?

For optimal performance, store the antibody at -20°C for long-term preservation. For short-term use (up to 2 weeks), storage at 4°C is acceptable . The antibody is typically supplied in phosphate buffered saline (without Mg²⁺ and Ca²⁺), pH 7.4, 150mM NaCl, 0.02% sodium azide, and 50% glycerol . Avoid repeated freeze-thaw cycles as they can degrade antibody quality.

What secondary antibodies are recommended for use with this antibody?

Since MET (Ab-1003) is a rabbit polyclonal antibody, anti-rabbit secondary antibodies are appropriate. Compatible options include:

  • Goat Anti-Rabbit IgG H&L Antibody (AP)

  • Goat Anti-Rabbit IgG H&L Antibody (Biotin)

  • Goat Anti-Rabbit IgG H&L Antibody (FITC)

  • Goat Anti-Rabbit IgG H&L Antibody (HRP)

The choice depends on your detection method and experimental design.

Can MET (Ab-1003) Antibody be used in multiplex immunostaining protocols?

Yes, the antibody can potentially be used in multiplex protocols, but requires careful optimization. When designing multiplex experiments:

  • Select secondary antibodies with minimal cross-reactivity

  • Consider using directly conjugated versions of the antibody

  • Validate the absence of signal bleed-through with single-stained controls

  • Use appropriate blocking steps to minimize background

How does MET (Ab-1003) Antibody compare to other MET antibodies for detecting specific alterations?

While MET (Ab-1003) Antibody detects total MET protein, researchers should consider whether this antibody is appropriate for their specific research focus. For MET exon 14 skipping mutations, which have emerged as actionable oncogenic alterations in NSCLC , specialized antibodies or detection methods might be required if the epitope is affected. When studying monovalent antibodies targeting MET for therapeutic applications, as in the case of onartuzumab , different detection strategies may be necessary.

Can MET (Ab-1003) Antibody distinguish between phosphorylated and non-phosphorylated forms of MET?

No, MET (Ab-1003) Antibody detects total MET protein regardless of phosphorylation status . The antibody targets a specific peptide sequence (V-D-Y-R-A) around amino acids 1001-1005 . If researchers need to distinguish phosphorylated forms, they should use antibodies specifically targeting phosphorylated epitopes, such as those recognizing phospho-tyrosine 1003.

How does fixation affect the performance of MET (Ab-1003) Antibody in IHC applications?

Fixation can significantly impact epitope accessibility. For formalin-fixed paraffin-embedded (FFPE) tissues, appropriate antigen retrieval methods are essential. The antibody has been successfully used on FFPE samples in research settings , but researchers should optimize fixation time and antigen retrieval protocols for their specific tissues.

What are the expected molecular weight bands when using MET (Ab-1003) Antibody in Western blotting?

When performing Western blot analysis, researchers should expect:

  • Full-length MET precursor: ~170 kDa

  • Processed β-chain: ~145 kDa

  • Processed α-chain: ~50 kDa (if using reducing conditions)

The expected banding pattern can be observed in Western blot analysis of HepG2 cells as demonstrated in validation studies .

How do I interpret different staining patterns observed with MET (Ab-1003) Antibody?

MET staining patterns may vary by cell type and activation status:

  • Membranous staining: Indicates receptor localization at the cell surface

  • Cytoplasmic staining: May indicate internalized receptor following activation

  • Heterogeneous staining: May reflect varying expression levels in different cell populations

In published immunohistochemical staining of human brain tissue, the antibody showed specific staining patterns consistent with MET expression .

What are common troubleshooting strategies for weak or non-specific staining?

For weak staining:

  • Increase antibody concentration (staying within recommended ranges)

  • Optimize antigen retrieval methods

  • Extend primary antibody incubation time

  • Use a more sensitive detection system

For non-specific staining:

  • Increase blocking time and concentration

  • Reduce primary antibody concentration

  • Include additional washing steps

  • Verify secondary antibody specificity

How can I quantify MET expression levels using MET (Ab-1003) Antibody?

For Western blot quantification:

  • Use densitometry software for band intensity analysis

  • Normalize to appropriate loading controls (GAPDH, β-actin)

For IHC/IF quantification:

  • Implement an established scoring system (0-3+ scale)

  • Consider the H-score method (combining intensity and percentage of positive cells)

  • Use digital image analysis software for objective quantification

Several MET IHC scoring systems have been published, with staining intensities commonly classified as negative (0), weak (1+), moderate (2+), and strong (3+), with 2+ staining in at least 50% of tumor cells often classified as MET overexpression .

How does MET (Ab-1003) Antibody compare to therapeutic anti-MET antibodies?

MET (Ab-1003) Antibody is designed for research applications to detect endogenous MET protein. In contrast, therapeutic antibodies like onartuzumab (MetMAb) are engineered as monovalent antibodies to prevent MET dimerization and activation . While bivalent antibodies produced agonists of MET, engineering them into monovalent antibodies created antagonists . This fundamental difference highlights that research antibodies and therapeutic antibodies serve different purposes and have different molecular designs.

What role does MET play in cancer research and how can MET (Ab-1003) Antibody support these studies?

MET plays crucial roles in cancer progression, particularly in:

  • Non-small cell lung cancer with MET exon 14 skipping mutations

  • Cancer resistance to targeted therapies (e.g., EGFR inhibitors)

  • Tumor metastasis and invasion

MET (Ab-1003) Antibody can support these research areas by:

  • Detecting MET expression in patient samples and cell lines

  • Monitoring MET levels in response to therapeutic interventions

  • Evaluating MET expression in various cancer models

  • Correlating MET expression with other biomarkers or clinical outcomes

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