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Phospho-Met (Tyr1234/1235) Recombinant Rabbit mAb (S-3260)

Phospho-Met (Tyr1234/1235) Recombinant Rabbit mAb (S-3260)

Catalog Number: S0B6873 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 (Tyr1234/1235)
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-3260
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 (Tyr1234/1235) refers to the activated form of the c-Met receptor tyrosine kinase, a critical transmembrane protein encoded by the MET proto-oncogene, wherein phosphorylation at tyrosine residues 1234 and 1235 within the intracellular kinase activation loop serves as a definitive molecular switch for its enzymatic activity. This specific dual phosphorylation event is induced upon binding of its primary ligand, hepatocyte growth factor (HGF), leading to conformational changes that stabilize the active kinase state, thereby facilitating downstream signal transduction through major pathways such as PI3K/Akt, RAS/MAPK, and STAT, which collectively regulate essential cellular processes including proliferation, survival, motility, and morphogenesis. Due to its pivotal role in tissue regeneration and embryonic development, as well as its frequent dysregulation in various malignancies where it drives tumor growth, invasion, and metastasis, Phospho-Met (Tyr1234/1235) is widely utilized as a specific biomarker in research and clinical diagnostics to monitor c-Met pathway activation and to evaluate the efficacy of targeted therapeutic inhibitors designed to block this oncogenic signaling axis.