TEK, TEK receptor tyrosine kinase, 7010

N. diseases: 300; N. variants: 17
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 AlteredExpression disease BEFREE Activation of Tie2 seems to accelerate recovery of the eGC and might hold promise as a therapeutic target in human sepsis. 31493777 2019
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE Tie2 suppression is a pivotal event in sepsis that may be regulated both by matrix metalloprotease 14-driven Tie2 protein cleavage and GATA binding protein 3-driven flow regulation of Tie2 transcript. 29979219 2018
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE In this review, we summarize how the Ang/Tie2 pathway is implicated in sepsis and describe its prognostic as well as therapeutic utility in life-threatening infections. 29740443 2018
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE Tie2 activation by angiopoietin-1 reduces, whereas Tie2 blockade by angiopoietin-2 increases, inflammation and permeability during sepsis. 29447449 2018
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 GeneticVariation disease BEFREE This study provides new evidence linking the Angiopoietin-Tie2 pathway with mortality and bacteremia in young infants with suspected sepsis. 29571293 2018
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE Angiopoietin-1 (Ang-1)-mediated Tie2 activation reduces, and the Ang-1 antagonist Ang-2 increases, inflammation and endothelial permeability in sepsis. 29132435 2017
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 PosttranslationalModification disease BEFREE Vascular inflammation and leakage in sepsis is mediated by Angiopoietin-1 (Ang-1) and Angiopoietin-2 (Ang-2) and their phosphorylation of the endothelial Tie-2 receptor. 28538018 2017
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE Targeting Tie2 and the host vascular response in sepsis. 27099172 2016
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE Wild-type (WT), EPCR knockout (KO) and Tie2-EPCR mice, which overexpress EPCR on the endothelium, were infected intranasally (pneumonia) or intravenously (sepsis) with viable Streptococcus pneumoniae and euthanised at 24 or 48 hours after initiation of the infection for analyses. 24401906 2014
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 AlteredExpression disease BEFREE Changes in Tie2 expression during sepsis development may contribute to microvascular dysfunction. 23563632 2013
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE This review summarizes results from cell-based experiments, animal models, and observational human studies; together, these studies suggest that an endothelial receptor called Tie2 and its ligands, called angiopoietins, form a signaling axis key to the vascular dyshomeostasis that underlies sepsis. 23652985 2013
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE This study adds to the evidence that the angiopoietin/Tie-2 axis represents a modifiable pathway through which targeted therapy may be able to directly reverse part of the pathology of sepsis. 23171759 2012
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 Biomarker disease BEFREE Increasing evidence suggests that the function of the vessel-protective factor Angiopoietin-1 (Ang-1), a ligand of the endothelial-specific Tie2 receptor, is inhibited by its antagonist Angiopoietin-2 (Ang-2) during sepsis. 21531574 2011
CUI: C0036690
Disease: Septicemia
Septicemia
0.100 AlteredExpression disease BEFREE We conclude that in vivo endotoxemia triggers functional inhibition of the Ang-1/Tie-2 receptor pathway by reducing Ang-1 and Tie-2 expression and inducing Ang-2 levels and that this response may contribute to enhanced vascular leakage in sepsis. 18310225 2008