ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 13 (ADAMTS13) ELISA Kits

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

1. ADAMTS-13 level was decreased in children with severe typical HUS and its deficiency correlated with disease severity.

2. A novel insight into mechano-chemical regulation on interaction between ADAMTS13 and vWF A2 domain under forces is provided.

3. higher VWF and low ADAMTS13 activity are associated with increased risk of dementia

4. Data confirm the critical role of exosite engagement for substrates to gain access to the active site of ADAMTS13, and define the substrate recognition motif for ADAMTS13.

5. Trp(390) residue within the WXXW motif is required for ADAMTS13 secretion and enzymatic activity

6. ADAMTS13 open-closed conformations regulate the activity of this highly specific VWF cleaving protease in thrombotic thrombocytopenic purpura [review]

7. analysis of a follow-up study showing higher mortality or thrombotic complications and increased platelet count, increased VWF:Ag levels and decreased ADAMTS13 activity in colorectal cancer

8. relative plasma deficiency of ADAMTS13 activity may be associated with more severe traumatic injury, significant endothelial glycocalyx damage, coagulation abnormalities and mortality after severe trauma in paediatric patients

9. Low ADAMTS-13 activity is a predictor of unfavourable outcome in patients with ischaemic stroke undergoing endovascular therapy

10. analysis of ADAMTS13 variants in a patient cohort with Upshaw-Schulman Syndrome investigated in Germany

11. Through its action on VWF, ADAMTS13 can have prothrombotic and proinflammatory properties, not only when its activity is severely deficient, but also when it is only moderately low.

12. An open ADAMTS-13 conformation is also a hallmark of acute acquired thrombotic thrombocytopenic purpura, altering autoantibody binding.

13. truncation of ADAMTS13 by plasmin abolishes intramolecular self-association, which improves interaction with unfolded von Willebrand Factor

14. antigen and activity both positively correlated with plasma viral load in HIV infection

15. protein C and ADAMTS-13 change were associated with outcome in an ongoing endothelial/hemostatic disorder was during sepsis

16. Upshaw-Schulman Syndrome With c.2728C>T Mutation in ADAMTS13 Gene.

17. ADAMTS13 rs2285489 genotyping in transplant recipients may be a useful tool for evaluating pretransplantation risks.

18. Genetic analysis of 5 children with congentical thrombotic thrombocytopenia purpura showed complex heterozygous mutations at different loci of ADAMTS13 gene

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

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

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

1. ADAMTS13 knockout promotes the occurrence of early brain injury after experimental subarachnoid hemorrhage.

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

3. Adamts13 deficiency in obese mice promotes hepatic microthrombosis.

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

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

6. 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

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

8. 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.

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

10. ADAMTS13 substrate specificity

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

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

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

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

15. 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)

16. 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.

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

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

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

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