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TEK (TIE2) is a receptor tyrosine kinase expressed almost exclusively in endothelial cells. It plays a central role in vascular stability and development. Activation by angiopoietins, particularly Ang1, initiates downstream signaling cascades affecting morphogenesis, proliferation, survival, differentiation, permeability regulation, and extracellular matrix interactions. It is critical for communication between endothelial cells and smooth muscle cells during venous morphogenesis, and is also involved in lymphatic vessel formation. Dysregulation or mutations in TIE2 are associated with venous malformations, tumor angiogenesis, and congenital glaucoma.
TIE2 is activated by angiopoietins (Ang1, Ang2, Ang4), primarily Ang1, leading to receptor dimerization/oligomerization and autophosphorylation. This recruits effector molecules for downstream signaling cascades controlling morphogenesis, proliferation, survival, differentiation, permeability regulation, and extracellular matrix interactions. Ang2 acts as a context-dependent antagonist or partial agonist.
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