TIE2/CD202b Polyclonal Antibody, ALEXA FLUOR® 750 Conjugated

Applications

  • FCM
  • IF(IHC-P)
  • IF(IHC-F)
  • IF(ICC)

Reactivity

  • Human
  • Mouse
  • Rat
  • Bovine

Predicted Reactivity

  • Cow
  • Pig
  • Horse
Overview
Catalog # bs-1300R-A750
Product Name TIE2/CD202b Polyclonal Antibody, ALEXA FLUOR® 750 Conjugated
Applications FCM, IF(IHC-P), IF(IHC-F), IF(ICC)
Reactivity Human, Mouse, Rat, Bovine
Predicted Reactivity Cow, Pig, Horse
Specifications
Conjugation ALEXA FLUOR® 750
Host Rabbit
Source KLH conjugated synthetic peptide derived from human Tie2
Immunogen Range 401-550/1120
Clonality Polyclonal
Isotype IgG
Concentration 1ug/ul
Purification Purified by Protein A.
Storage Buffer Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage Condition Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles.
Target
Gene ID 7010
Swiss Prot Q02763
Subcellular location Cytoplasm, Secreted, Cell membrane
Synonyms TIE2; VMCM; TIE-2; VMCM1; CD22B; Angiopoietin-1 receptor; Endothelial tyrosine kinase; Tunica interna endothelial cell kinase; Tyrosine kinase with Ig and EGF homology domains-2; Tyrosine-protein kinase receptor TEK; Tyrosine-protein kinase receptor TIE-2; hTIE2; p14 TEK; TEK
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.
Application Dilution
FCM 1:20-100
IF(IHC-P) 1:50-200
IF(IHC-F) 1:50-200
IF(ICC) 1:50-200