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studies demonstrate that pRb (show PGR Proteins) loss in the Tie2-lineage that includes aortic valve interstitial cells is sufficient to cause age-dependent aortic valve dysfunction
Together, these results imply that Tie2 is essential for venous specification and maintenance via Akt (show AKT1 Proteins) mediated stabilization of COUP-TFII (show NR2F2 Proteins).
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.
TEK mutations have a role in primary congenital glaucoma with variable expressivity
ANG2 activation of Tie2 supports stable enlargement of normal nonleaky vessels, but reduction of Tie1 in inflammation leads to ANG2 antagonism of Tie2 and initiates a positive feedback loop wherein FOXO1-driven ANG2 expression promotes vascular remodeling and leakage
Hydroxysafflor yellow A promotes angiogenesis in ischemic hindlimb via the angiopoietin 1 (show ANGPT1 Proteins)/ Tie-2 signaling pathway.
TBMS1 further stimulated the proteasomal degradation of vascular endothelial growth factor receptor-2 (VEGFR2 (show KDR Proteins)) and Tie2 in endothelial cells, which down-regulated AKT (show AKT1 Proteins)/mTOR (show FRAP1 Proteins) signaling.
results implicate common genetic variation at the TIE2 locus as a determinant of vascular leak-related clinical outcomes from common infections, suggesting new tools to identify individuals at unusual risk for deleterious complications of infection
the results suggest that an increased level of TNF-alpha (show TNF Proteins) together with concomitant upregulation of Tie2/Angiopoietin signaling have critical roles in severe dengue infection.
Data support an interactive model of Tie1 (show TIE1 Proteins) and Tie2 function, in which dynamically regulated Tie1 (show TIE1 Proteins) versus Tie2 expression determines the net positive or negative effect of Tie1 (show TIE1 Proteins) on Tie2 signaling.
We demonstrate that ANGPT2 (show ANGPT2 Proteins) 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.
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 (show ANGPT1 Proteins) and Angiopoietin-2 (show ANGPT2 Proteins), regulate its activation status.
Ang-2 (show ANGPT2 Proteins) and sTie-2 plasma levels are increased in pediatric OSA and obesity, particularly when endothelial dysfunction or insulin (show INS Proteins) resistance is detectable.
IL-6 (show IL6 Proteins) and TIE2 polymorphisms are associated with baseline peritoneal transport property.
Results show that TIE2 phosphorylates caveolin-1 (show CAV1 Proteins) at Tyr14, and associates with caveolin-1 (show CAV1 Proteins) in caveolae. Also, its nuclear translocation is caveolin-1 (show CAV1 Proteins) dependent.
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
ANG-1 (show ANGPT1 Proteins), ANG-2 (show ANGPT2 Proteins) and TIE-2 levels were significantly increased in placenta of non-complicated ART pregnancies compared to placentas from spontaneous conception.
Our data suggest that interaction of TEK and CYP1B1 (show CYP1B1 Proteins) contributes to primary congenital glaucoma pathogenesis and argue that TEK-CYP1B1 (show CYP1B1 Proteins) may perform overlapping as well as distinct functions in manifesting the disease etiology.
Angiopoietin-1 receptor Tie2 distinguishes multipotent differentiation capability in bovine coccygeal nucleus pulposus cells.
observations demonstrate that Tie2 is an important regulator of tip cell behaviors
Tie-1 (show TIE1 Proteins) and Tie-2 are not required for early heart development, yet they have redundant roles for the maintenance of endocardial-myocardial connection in later stages.
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.
growth factor receptor Tie2/Tek
, TEK tyrosine kinase, endothelial (venous malformations, multiple cutaneous and mucosal)
, Angiopoietin-1 receptor
, TEK tyrosine kinase, endothelial
, angiopoietin-1 receptor-like
, angiopoietin-1 receptor
, endothelial tyrosine kinase
, p140 TEK
, 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
, soluble TIE2 variant 1
, soluble TIE2 variant 2
, protein-tyrosine kinase Tie2
, endothelial-specific receptor tyrosine kinase
, tyrosine kinases that contain immunoglobulin-like loops and epidermal growth factor-similar domains 2
, endothelium-specific receptor tyrosine kinase 2
, tyrosine-protein kinase receptor Tie-2