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the relation of Ang2 and Tie2 with inflammation markers in the general population, was examined.
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Tie2 is the first, validated, tumor vascular response biomarker for VEGF inhibitors.
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Tie2-expressing pericytes limit in a paracrine manner endothelial cell sprouting angiogenesis.
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Although several lines of evidences indicate that the Tie2 pathway might have a role in asthma, the investigated variations in the TEK gene, which are associated with lower Tie2 expression, did not influence the susceptibility to the disease. However, we found that the homozygote carriers of the rs581724 SNP had significantly increased risk to allergic conjunctivitis.
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Under up-regulation of TIE2-R849W, egfl7 could be considered a potential reason for venous defects. Moreover, the wnt pathway may perform an important role as a key trigger for head multi-malformations.
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TIE2 mutation type in VM, especially the mutation site, is important for future targeted therapies.
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Rebastinib inhibition of angiopoietin/Tie2 signaling impairs multiple pathways in tumor progression mediated by protumoral Tie2(+) macrophages, including TMEM-dependent dissemination and angiopoietin/Tie2-dependent angiogenesis. Rebastinib is a promising therapy for achieving Tie2 inhibition in cancer patients.
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Angiopoietin-2 acts as a survival factor for chronic lymphocytic leukemia B cells throughout Tie-2 receptor engagement.
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mutations in the germline and somatic DNA of the TEK gene were identified and analyze the expression level of Src and phospho-Src (p-Src) in tumor and healthy tissues from patients with facial cutaneo-mucosal venous malformations.
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We demonstrate that ANGPT2 signaling activated after estrogen depletion paradoxically triggers ER+ tumor cell awakening from dormancy in their BM niche, partly indirectly via endothelial Tie2 receptor and partly directly via tumor cell surface integrin &1.
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When Tie2 becomes inactivated, important molecular brakes are released in the endothelium, which in turn potentiate inflammation and vascular leakage. The ligands of Tie2, Angiopoietin-1 and Angiopoietin-2, regulate its activation status.
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Ang-2 and sTie-2 plasma levels are increased in pediatric OSA and obesity, particularly when endothelial dysfunction or insulin resistance is detectable.
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IL-6 and TIE2 polymorphisms are associated with baseline peritoneal transport property.
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Results show that TIE2 phosphorylates caveolin-1 at Tyr14, and associates with caveolin-1 in caveolae. Also, its nuclear translocation is caveolin-1 dependent.
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These results indicate that the Angpt-Tie2 system is essential for SC integrity. The impairment of this system underlies POAG-associated pathogenesis, supporting the possibility that Tie2 agonists could be a therapeutic option for glaucoma.
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TEK mutations have a role in primary congenital glaucoma with variable expressivity
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Tie1 directly interacts with Tie2 to promote ANG-induced vascular responses under noninflammatory conditions, whereas in inflammation, Tie1 cleavage contributes to loss of ANG2 agonist activity and vascular stability
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ANG-1, ANG-2 and TIE-2 levels were significantly increased in placenta of non-complicated ART pregnancies compared to placentas from spontaneous conception.
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Our data suggest that interaction of TEK and CYP1B1 contributes to primary congenital glaucoma pathogenesis and argue that TEK-CYP1B1 may perform overlapping as well as distinct functions in manifesting the disease etiology.
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High Tie-2 expression is associated with Primary Myelofibrosis.
