免 疫 原：KLH conjugated Synthesised phosphopeptide derived from human TIE2 around the phosphorylation site of Tyr1108
抗原表位：TL(p-Y)EK
SWISS：Q02763
Gene ID ：7010
Human Gene ID：7010

The TEK receptor tyrosine kinase is expressed almost exclusively in endothelial cells in mice, rats, and humans. This receptor possesses a unique extracellular domain containing 2 immunoglobulin-like loops separated by 3 epidermal growth factor-like repeats that are connected to 3 fibronectin type III-like repeats. The ligand for the receptor is angiopoietin-1. Defects in TEK are associated with inherited venous malformations; the TEK signaling pathway appears to be critical for endothelial cell-smooth muscle cell communication in venous morphogenesis.TEK is closely related to the TIE receptor tyrosine kinase.
Function：This protein is a protein tyrosine-kinase transmembrane receptor for angiopoietin 1. It may constitute the earliest mammalian endothelial cell lineage marker. Probably regulates endothelial cell proliferation, differentiation and guides the proper pattern
Subunit：Homodimer. Heterodimer with TIE1. Interacts with ANGPT1, ANGPT2 and ANGPT4. At cell-cell contacts in quiescent cells, forms a signaling complex composed of ANGPT1 plus TEK molecules from two adjoining cells. In the absence of endothelial cell-cell contact
Subcellular Location：Cell membrane; Single-pass type I membrane protein. Cell junction. Cell junction, focal adhesion. Cytoplasm, cytoskeleton. Secreted. Note=Recruited to cell-cell contacts in quiescent endothelial cells. Colocalizes with the actin cytoskeleton and at actin
Tissue Specificity：Predominantly expressed in endothelial cells and their progenitors, the angioblasts. Has been directly found in placenta and lung, with a lower level in umbilical vein endothelial cells, brain and kidney.
Post-translational modifications：Phosphorylated. Phosphorylation is induced by ANGPT1 and ANGPT2. ANGPT1-induced phosphorylation is impaired during hypoxia. Dephosphorylated by PTPRB.
Autophosphorylation at Tyr-1108 is critical for coupling downstream cell migration signal transducti
DISEASE：Defects in TEK are a cause of dominantly inherited venous malformations (VMCM) [MIM:600195]; an error of vascular morphogenesis characterized by dilated, serpiginous channels.
Similarity：Belongs to the protein kinase superfamily.
Tyr protein kinase family. Tie subfamily.
Contains 3 EGF-like domains.
Contains 3 fibronectin type-III domains.
Contains 2 Ig-like C2-type (immunoglobulin-like) domains.
Contains 1 protein kin
Important Note：This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.