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Phospho-Met (Tyr1349) Recombinant Rabbit mAb (S-3345)

Phospho-Met (Tyr1349) Recombinant Rabbit mAb (S-3345)

Catalog Number: S0B6874 Application: WB Reactivity: Hu, Ms, Rt Conjugation: Unconjugated Brand: Starter
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Regular price $100 USD
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Product Details

Product Specification


Host Rabbit
Antigen Phospho-Met (Tyr1349)
Synonyms Hepatocyte growth factor receptor; HGF/SF receptor; Proto-oncogene c-Met; Scatter factor receptor (SF receptor); Tyrosine-protein kinase Met; MET
Location Membrane
Accession P08581
Clone Number S-3345
Antibody Type Recombinant mAb
Isotype IgG
Application WB
Reactivity Hu, Ms, Rt
Purification Protein A
Concentration 0.5 mg/ml
Conjugation Unconjugated
Physical Appearance Liquid
Storage Buffer

PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300

Stability & Storage

12 months from date of receipt / reconstitution, -20 °C as supplied

Dilution


application dilution species
WB 1:1000 Hu, Ms, Rt

Background

Phospho-Met (Tyr1349) refers to a critical phosphorylation modification at the C-terminal multifunctional docking site of the hepatocyte growth factor receptor (MET, a receptor tyrosine kinase), specifically the phosphorylation of tyrosine residue 1349. Upon binding of hepatocyte growth factor (HGF) to MET, MET dimerizes and undergoes autophosphorylation; once phosphorylated, Tyr1349 forms a stable characteristic "pYXNXXV" motif, acting directly as a high-affinity docking site for multiple downstream signaling effector proteins (such as GAB1, GRB2, SHC, and the p85 subunit of PI3K). This phosphorylation event serves as a central hub for activating several key signaling pathways, including Ras-MAPK (promoting cell proliferation), PI3K-Akt (promoting cell survival and migration), and PLCγ-Ca²⁺ (regulating cell morphology). Physiologically, it precisely regulates embryonic development, tissue regeneration, and synaptogenesis. Pathologically, hyperphosphorylation or sustained activation of Tyr1349 is commonly observed in various cancers (e.g., non-small cell lung cancer, gastric cancer, and colorectal cancer), driving aggressive tumor growth, epithelial-mesenchymal transition (EMT), and drug resistance through the recruitment of adaptor proteins such as GAB1.