Met Antibody [K15N1] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat, Monkey

Usage Information

Dilution
WB1:1000 IP1:50

Application
WB, IP

Reactivity
Human, Mouse, Rat, Monkey

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
145, 170 kDa

Positive Control	HeLa cells; mIMCD3 cells; 293 (starved); C6 cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
Met Antibody [K15N1] detects endogenous levels of total Met protein.

Clone
K15N1

Synonym(s)
Hepatocyte growth factor receptor; HGF receptor; HGF/SF receptor; Proto-oncogene c-Met; Scatter factor receptor (SF receptor); Tyrosine-protein kinase Met; MET

Background
MET (also known as c-MET or hepatocyte growth factor receptor) is a receptor tyrosine kinase (RTK) that functions as a disulfide-linked heterodimer, composed of an extracellular α-chain and a transmembrane β-chain. It is crucial for embryonic development, wound healing, and tissue regeneration, primarily through its high-affinity binding to hepatocyte growth factor (HGF, also known as scatter factor). MET features an extracellular Sema domain, a seven-bladed β-propeller responsible for HGF engagement, followed by PSI and four IPT domains that confer ligand specificity and stability. The receptor crosses the membrane via a single-pass helix and contains an intracellular juxtamembrane segment, a tyrosine kinase domain with key activation loop tyrosines (Tyr1234 and Tyr1235), and a C-terminal tail with important docking sites such as Tyr1349 (essential for adaptor recruitment like Gab1) and Tyr1003 (a site for c-Cbl-mediated ubiquitination). Upon HGF binding, MET dimerizes and undergoes sequential autophosphorylation: first at Tyr1234/1235 for kinase activation, followed by phosphorylation of additional sites (e.g., Tyr1349), which serve as platforms for recruiting signaling adaptors like Gab1/2, Grb2, PI3K, PLCγ, and STAT3. These interactions activate multiple downstream pathways including PI3K/AKT (cell survival and migration), RAS-MAPK (proliferation), FAK/Src/integrin (motility and invasion), and STAT (differentiation). Phosphorylation at Tyr1003 enables c-Cbl-mediated ubiquitination, leading to receptor endocytosis and lysosomal degradation for signal attenuation. MET is essential for organogenesis processes such as hepatogenesis, myogenesis, nephrogenesis, and for maintaining adult tissue homeostasis, particularly by driving epithelial-mesenchymal transitions (EMT) during morphogenesis and tissue repair. Aberrant MET activation, resulting from gene amplification, activating mutations (especially in kinase domain hotspots), HGF overexpression, or autocrine/paracrine loops, contributes to oncogenesis in various cancers (e.g., non-small cell lung cancer, gastric, renal, hepatocellular carcinoma). This leads to sustained proliferation, invasion, metastasis, angiogenesis (partly via VEGF), and resistance to therapies such as EGFR tyrosine kinase inhibitors.

Background

MET (also known as c-MET or hepatocyte growth factor receptor) is a receptor tyrosine kinase (RTK) that functions as a disulfide-linked heterodimer, composed of an extracellular α-chain and a transmembrane β-chain. It is crucial for embryonic development, wound healing, and tissue regeneration, primarily through its high-affinity binding to hepatocyte growth factor (HGF, also known as scatter factor). MET features an extracellular Sema domain, a seven-bladed β-propeller responsible for HGF engagement, followed by PSI and four IPT domains that confer ligand specificity and stability. The receptor crosses the membrane via a single-pass helix and contains an intracellular juxtamembrane segment, a tyrosine kinase domain with key activation loop tyrosines (Tyr1234 and Tyr1235), and a C-terminal tail with important docking sites such as Tyr1349 (essential for adaptor recruitment like Gab1) and Tyr1003 (a site for c-Cbl-mediated ubiquitination). Upon HGF binding, MET dimerizes and undergoes sequential autophosphorylation: first at Tyr1234/1235 for kinase activation, followed by phosphorylation of additional sites (e.g., Tyr1349), which serve as platforms for recruiting signaling adaptors like Gab1/2, Grb2, PI3K, PLCγ, and STAT3. These interactions activate multiple downstream pathways including PI3K/AKT (cell survival and migration), RAS-MAPK (proliferation), FAK/Src/integrin (motility and invasion), and STAT (differentiation). Phosphorylation at Tyr1003 enables c-Cbl-mediated ubiquitination, leading to receptor endocytosis and lysosomal degradation for signal attenuation. MET is essential for organogenesis processes such as hepatogenesis, myogenesis, nephrogenesis, and for maintaining adult tissue homeostasis, particularly by driving epithelial-mesenchymal transitions (EMT) during morphogenesis and tissue repair. Aberrant MET activation, resulting from gene amplification, activating mutations (especially in kinase domain hotspots), HGF overexpression, or autocrine/paracrine loops, contributes to oncogenesis in various cancers (e.g., non-small cell lung cancer, gastric, renal, hepatocellular carcinoma). This leads to sustained proliferation, invasion, metastasis, angiogenesis (partly via VEGF), and resistance to therapies such as EGFR tyrosine kinase inhibitors.

References
https://pubmed.ncbi.nlm.nih.gov/33860789/ https://pubmed.ncbi.nlm.nih.gov/19861919/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%