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

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

价格 600.00 供应商现货 : 3-5个工作日
货号 S0B6874
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产品介绍 评论(0)

产品规格
  • 宿主来源

    Rabbit
  • 抗原名称

    Phospho-Met (Tyr1349)
  • 分子别名

    Hepatocyte growth factor receptor; HGF/SF receptor; Proto-oncogene c-Met; Scatter factor receptor (SF receptor); Tyrosine-protein kinase Met; MET
  • 细胞定位

    Membrane
  • Accession

    P08581
  • 克隆号

    S-3345
  • 抗体类型

    Recombinant mAb
  • 抗体同种型

    IgG
  • 反应种属 ?

    Hu, Ms, Rt
  • 纯化方式

    Protein A
  • 浓度

    0.5 mg/ml
  • 标记

    Unconjugated
  • 性状

    Liquid
  • 缓冲体系

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

  • 储存条件

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

  • 应用

    WB

  • 稀释度

    应用 稀释度 推荐种属
    WB 1:1000 Hu, Ms, Rt
背景介绍
  • 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.

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