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Your Position: Home > All Other Proteins > TIE2 > TI2-C5253

Cynomolgus TIE2 Protein, His Tag

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  • Synonym
    TIE2,Tie-2,TEK,VMCM, VMCM1,CD202b,Angiopoietin-1 receptor
  • Source
    Cynomolgus TIE2, Fc Tag (TI2-C5253) is expressed from human 293 cells (HEK293). It contains AA Ala 23 - Lys 745 (Accession # A0A2K5VRI3-1).
    Predicted N-terminus: Ala 23
  • Molecular Characterization
    Online-Res(Ala 23 - Lys 745) A0A2K5VRI3-1

    This protein carries a polyhistidine tag at the C-terminus.

    The protein has a calculated MW of 82.5 kDa.

  • Endotoxin
  • Formulation

    Please contact us for detailed information.

    Contact us for customized product form or formulation.

  • Reconstitution

    Please see Certificate of Analysis for specific instructions.

    For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

  • Storage

    For long term storage, the product should be stored at lyophilized state at -20°C or lower.

    Please avoid repeated freeze-thaw cycles.

    This product is stable after storage at:

    1. -20°C to -70°C for 12 months in lyophilized state;
    2. -70°C for 3 months under sterile conditions after reconstitution.
  • Background
    Tyrosine-protein kinase that acts as cell-surface receptor for ANGPT1, ANGPT2 and ANGPT4 and regulates angiogenesis, endothelial cell survival, proliferation, migration, adhesion and cell spreading, reorganization of the actin cytoskeleton, but also maintenance of vascular quiescence. Has anti-inflammatory effects by preventing the leakage of proinflammatory plasma proteins and leukocytes from blood vessels. Required for normal angiogenesis and heart development during embryogenesis. Required for post-natal hematopoiesis. After birth, activates or inhibits angiogenesis, depending on the context. Inhibits angiogenesis and promotes vascular stability in quiescent vessels, where endothelial cells have tight contacts. In quiescent vessels, ANGPT1 oligomers recruit TEK to cell-cell contacts, forming complexes with TEK molecules from adjoining cells, and this leads to preferential activation of phosphatidylinositol 3-kinase and the AKT1 signaling cascades. In migrating endothelial cells that lack cell-cell adhesions, ANGT1 recruits TEK to contacts with the extracellular matrix, leading to the formation of focal adhesion complexes, activation of PTK2/FAK and of the downstream kinases MAPK1/ERK2 and MAPK3/ERK1, and ultimately to the stimulation of sprouting angiogenesis. ANGPT1 signaling triggers receptor dimerization and autophosphorylation at specific tyrosine residues that then serve as binding sites for scaffold proteins and effectors. Signaling is modulated by ANGPT2 that has lower affinity for TEK, can promote TEK autophosphorylation in the absence of ANGPT1, but inhibits ANGPT1-mediated signaling by competing for the same binding site. Signaling is also modulated by formation of heterodimers with TIE1, and by proteolytic processing that gives rise to a soluble TEK extracellular domain. The soluble extracellular domain modulates signaling by functioning as decoy receptor for angiopoietins. TEK phosphorylates DOK2, GRB7, GRB14, PIK3R1; SHC1 and TIE1.
  • Clinical and Translational Updates
      
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Price(USD) : $1980.00

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  • Number of Launched Drugs:4 Details
  • Number of Drugs in Clinical Trials:7 Details
  • Latest Research Phase:Approved

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