anti-TEK (TEK) 抗体产品概述

Mouse (Murine) TEK Tyrosine Kinase, Endothelial (TEK) interaction partners

1. Late gestational deletion of the angiopoietin receptor endothelial tyrosine kinase 2 (Tie2) or both angiopoietin-1 and angiopoietin-2 prevents ascending vasa recta formation in mice. The AVRs are Tie2 signaling-dependent specialized hybrid vessels.

2. Tie2 activation had no adverse effects on bleeding. These results mechanistically implicate Tie2 signaling as a central regulator of microvascular thrombus formation in septic DIC and indicate that circulating markers of the Tie2 axis could facilitate earlier diagnosis.

3. The Ang1/Tie2 system cross-talks with integrin alpha5beta1 in brain endothelial cells after cerebral ischemia.

4. constant endothelial activation by transmembrane tumor necrosis factor-alpha (tmTNF-alpha) exacerbates age-induced visual deficits via senescence-mediated ER stress in a transgenic model

5. Tie2 deletion in pericytes transiently delays postnatal retinal angiogenesis, yet results in a pronounced pro-angiogenic effect leading to enhanced tumour growth.

6. ANGPT2-TIE2 signaling is essential for mesenteric lymphatic development.VEPTP (vascular endothelial protein tyrosine phosphatase) determines TIE2 response to ANGPT2.

7. Data (including data from studies in transgenic mice) suggest that Dkk2 secreted from pericytes promotes angiogenesis and neurogenesis/neural regeneration via Angpt1/Tie2/Wnt signaling; here, overexpression of Dkk2 in diabetic mice enhances penile angiogenesis/neural regeneration and restores erectile function. (Dkk2 = dickkopf-2; Angpt1= angiopoietin-1; Tie2 = endothelial-specific receptor tyrosine kinase Tie2)

8. Angiopoietin-1/Tek vascular growth factor system leads to increased metastasis without affecting primary tumor growth.

9. these results demonstrated that RIPK3-mediated signaling in Tie-2 expressing cells was responsible for the embryonic lethality of Fadd-/- with cardiac failure.

10. studies demonstrate that pRb loss in the Tie2-lineage that includes aortic valve interstitial cells is sufficient to cause age-dependent aortic valve dysfunction

11. Together, these results imply that Tie2 is essential for venous specification and maintenance via Akt mediated stabilization of COUP-TFII.

12. 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.

13. TEK mutations have a role in primary congenital glaucoma with variable expressivity

14. 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

15. Hydroxysafflor yellow A promotes angiogenesis in ischemic hindlimb via the angiopoietin 1/ Tie-2 signaling pathway.

16. TBMS1 further stimulated the proteasomal degradation of vascular endothelial growth factor receptor-2 (VEGFR2) and Tie2 in endothelial cells, which down-regulated AKT/mTOR signaling.

17. 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

18. the results suggest that an increased level of TNF-alpha together with concomitant upregulation of Tie2/Angiopoietin signaling have critical roles in severe dengue infection.

19. Data support an interactive model of Tie1 and Tie2 function, in which dynamically regulated Tie1 versus Tie2 expression determines the net positive or negative effect of Tie1 on Tie2 signaling.

20. These results suggest that Tie2 signaling induces alpha4beta1 integrin activation on bone marrow-mast cell progenitor for adhesion to VCAM-1.

Human TEK Tyrosine Kinase, Endothelial (TEK) interaction partners

1. Tie2 activation had no adverse effects on bleeding. These results mechanistically implicate Tie2 signaling as a central regulator of microvascular thrombus formation in septic DIC and indicate that circulating markers of the Tie2 axis could facilitate earlier diagnosis.

2. serum level not influenced by pre-eclampsia with HIV infection

3. the relation of Ang2 and Tie2 with inflammation markers in the general population, was examined.

4. Tie2 is the first, validated, tumor vascular response biomarker for VEGF inhibitors.

5. Tie2-expressing pericytes limit in a paracrine manner endothelial cell sprouting angiogenesis.

6. 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.

7. 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.

8. TIE2 mutation type in VM, especially the mutation site, is important for future targeted therapies.

9. 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.

10. Angiopoietin-2 acts as a survival factor for chronic lymphocytic leukemia B cells throughout Tie-2 receptor engagement.

11. 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.

12. 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.

13. 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.

14. Ang-2 and sTie-2 plasma levels are increased in pediatric OSA and obesity, particularly when endothelial dysfunction or insulin resistance is detectable.

15. IL-6 and TIE2 polymorphisms are associated with baseline peritoneal transport property.

16. Results show that TIE2 phosphorylates caveolin-1 at Tyr14, and associates with caveolin-1 in caveolae. Also, its nuclear translocation is caveolin-1 dependent.

17. 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.

18. TEK mutations have a role in primary congenital glaucoma with variable expressivity

19. 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

20. ANG-1, ANG-2 and TIE-2 levels were significantly increased in placenta of non-complicated ART pregnancies compared to placentas from spontaneous conception.

Pig (Porcine) TEK Tyrosine Kinase, Endothelial (TEK) interaction partners

1. there might be an association between Tie receptors and intussusceptive angiogenesis during porcine metanephric development and during glomerulogenesis in particular

Cow (Bovine) TEK Tyrosine Kinase, Endothelial (TEK) interaction partners

1. Angiopoietin-1 receptor Tie2 distinguishes multipotent differentiation capability in bovine coccygeal nucleus pulposus cells.

Zebrafish TEK Tyrosine Kinase, Endothelial (TEK) interaction partners

1. observations demonstrate that Tie2 is an important regulator of tip cell behaviors

2. Tie-1 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.