Binds to TEK/TIE2, competing for the ANGPT1 binding site, and modulating ANGPT1 signaling. Can induce tyrosine phosphorylation of TEK/TIE2 in the absence of ANGPT1. In the absence of angiogenic inducers, such as VEGF, ANGPT2-mediated loosening of cell-matrix contacts may induce endothelial cell apoptosis with consequent vascular regression. In concert with VEGF, it may facilitate endothelial cell migration and proliferation, thus serving as a permissive angiogenic signal. Interacts with TEK/TIE2, competing for the same binding site as ANGPT1. 3 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Molecular Function: protein binding; metal ion binding; receptor tyrosine kinase binding; receptor binding
Biological Process: organ regeneration; Tie receptor signaling pathway; maternal process involved in pregnancy; negative regulation of blood vessel endothelial cell migration; signal transduction; response to organic cyclic substance; germ cell development; negative regulation of positive chemotaxis; positive regulation of angiogenesis; response to radiation; negative regulation of angiogenesis; response to mechanical stimulus; response to hypoxia; response to glucose stimulus; angiogenesis; response to activity; blood coagulation; leukocyte migration
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.