anti-ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 13 (ADAMTS13) Antikörper

Human ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 13 (ADAMTS13) Interaktionspartner

1. this study shows that in Upshaw-Schulman syndrome, age-onset defines two entities and ADAMTS13 sequence variations modify ADAMTS13 conformation

2. acute myeloid leukemia patients with low activity of ADAMTS-13 had worse prognosis after bone morrow transplantation.

3. The Plasma Levels of ADAMTS-13, von Willebrand Factor, VWFpp, and Fibrin-Related Markers in Patients With Systemic Sclerosis Having Thrombosis

4. The aim of the study was to investigate the role of von Willebrand factor (vWF), the vWF-cleaving protease, ADAMTS13, the composition of thrombus, and patient outcome following mechanical cerebral artery thrombectomy in patients with acute ischemic stroke.

5. ADAMTS 1, 4, 12, and 13 levels in the maternal and cord blood were lower in the preeclampsia group than in the control group. ADAMTS 1, 4, and 12 levels in placental tissues were higher in the preeclampsia group.

6. Decreased ADAMTS-13 activity was found in patients with proliferative lupus nephritis, and plasma ADAMTS-13 activity was closely associated with renal injury indices.

7. These results suggest that highly elevated plasma VWF might accelerate platelet thrombus formation not only in the circulation but also on the surface of vascular endothelial cells in the setting of ADAMTS13 deficiency in Upshaw-Schulman syndrome.

8. Prothrombotic state and systemic inflammation status might contribute to explaining the high incidence of concealed chronic renal failure in COPD, and plasma ADAMTS-13 levels may serve as a strong predictor.

9. VWF, GMP-140, ADAMTS13 and the cerebral vasospasm, delayed cerebral ischemia, tumor diameter and prognosis of aneurysmal subarachnoid hemorrhage patients are closely related

10. The levels of ADAMTS13 among neonates were higher as compared with healthy adults, despite a significant elevation of VWF antigen (Ag) and Ristocetin cofactor (RiCof) noted in all neonates.

11. investigated the roles of ADAMTS13 and VWF in thrombotic events of patients with Connective Tissue Diseases

12. Studied the significance of the von Willebrand factor (VWF)/ ADAMTS-13 ratio in advanced non-small-cell lung cancer (NSCLC). Findings suggest that the imbalance between VWF secretion and ADAMTS-13 may play a role in the hypercoagulability state in advanced NSCLC, and increase of the plasma VWF/ADAMTS-13 ratio may serve as an independent predictive factor for mortality in patients with advanced NSCLC.

13. vaso-occlusive crisis in sickle cell disease is associated with increased reactivity of VWF, without a pronounced ADAMTS-13 deficiency

14. The endogenous plasmin activation alone is not sufficient to cause Thrombotic thrombocytopenic purpura (TTP), but plasmin activation with ADAMTS13 deficiency might increase the risk of TTP onset.

15. the N-linked glycans of ADAMTS-13 play a crucial role in regulating ADAMTS-13 activity

16. Complex VWF-ADAMTS13-mediated mechanisms disturb haemostasis in inflammatory bowel disease.

17. Missense variant in ADAMTS13 gene in a patient with NCIPH decreases secretion and activity of ADAMTS13 protein.

18. Deficiency of the von Willebrand factor-cleaving protease ADAMTS13 is central to the pathophysiology of thrombotic thrombocytopenic purpura. Reviewed is the evidence emerged from epidemiological studies of an inverse relationship between the plasma levels of ADAMTS13 and the risk of acute coronary syndrome. [review]

19. Data indicate that in cultured endothelial cells, one role of endogenous ADAMTS-13 is regulation of angiogenesis, mediated through VEGF and AKT signaling pathway.

20. ADAMTS13 haplotype had an independent protective effect on CAD and genetic variation of vWF V1565L polymorphism modulates ADAMTS13 activity.

Mouse (Murine) ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 13 (ADAMTS13) Interaktionspartner

1. ADAMTS13-vWF axis is partially involved in the pathophysiology of kidney ischemic reperfusion injury.

2. Adamts13 deficiency in obese mice promotes hepatic microthrombosis.

3. results suggest that ADAMTS13 controls key steps of ischemic vascular remodeling and that recombinant ADAMTS13 is a putative therapeutic avenue for promoting stroke recovery.

4. ADAMTS13 retards progression of diabetic nephropathy, most likely by inhibiting VWF-dependent intrarenal thrombosis.

5. administration of ADAMTS13 5 minutes after occlusion dose-dependently dissolved these t-PA-resistant thrombi resulting in fast restoration of MCA patency and consequently reduced cerebral infarct sizes

6. Sleeping beauty transposon-mediated gene therapy achieved sustained expression of transgene ADAMTS13 and long-term prophylaxis against congenital thrombotic thrombocytopenic purpura in Adamts13(-/-) mice.

7. Results also suggest that Toxoplasma gondii-mediated apoptosis might play a pivotal role and a different type of role in the mechanism of neurodegeneration and neuropathology in the process of toxoplasma encephalitis. Furthermore, expression of ADAMTS-13 might give an idea of the progress and is critical for diagnosis of this disease.

8. Letter: deficiency of ADAMTS13 results in increased formation of venous thrombosis in mice.

9. ADAMTS13 substrate specificity

10. Data indicate that the p.D187H mutation impairs ADAMTS13 activity and secretion and may contribute to thrombotic thrombocytopenic purpura.

11. Data show that metalloendopeptidase ADAMTS13 does not directly promote development of adipose tissue.

12. findings provide further evidence on the pathophysiological role for the ADAMTS13/VWF axis in atherosclerosis

13. Carboxyl terminus of ADAMTS13 directly inhibits platelet aggregation and ultra large von Willebrand factor string formation under flow in a free-thiol-dependent manner.

14. Three novel mutations in a homozygous state were identified in these patients: c.1308G>C, c.428T>C (p.Ile143Thr) and c.1709A>G (p.Tyr570Cys)

15. The results indicate that the microvascular process induced by ADAMTS13 deficiency triggers complement activation on platelets and the endothelium, which may contribute to formation of thrombotic microangiopathy.

16. model of acute myocardial infarction in ADAMTS13 gene deleted (Adamts13 -/-) mice

17. We hypothesize that ADAMTS13 protects brain from ischemia-reperfusion injury by regulating von Willebrand factor -dependent inflammation as well as microvascular plugging

18. Cyclophilin B activity regulated secretion and activity of ADAMTS13.

19. Adamts13(-/-) mice developed larger myocardial infarctions than wild-type control mice.

20. ADAMTS13 and VWF are causally involved in myocardial ischemia/reperfusion injury.