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ADAMTS13 encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motif) protein family.
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Human Polyclonal ADAMTS13 Primary Antibody for WB - ABIN152016
Tao, Wang, Choi, Bernardo, Nishio, Sadler, López, Dong: Cleavage of ultralarge multimers of von Willebrand factor by C-terminal-truncated mutants of ADAMTS-13 under flow. in Blood 2005
Show all 5 Pubmed References
Human Polyclonal ADAMTS13 Primary Antibody for IP, WB - ABIN251718
Feng, Eyler, Zhang, Maga, Nester, Kroll, Smith, Afshar-Kharghan: Partial ADAMTS13 deficiency in atypical hemolytic uremic syndrome. in Blood 2013
Show all 2 Pubmed References
Human Polyclonal ADAMTS13 Primary Antibody for WB - ABIN251717
Turner, Nolasco, Ruggeri, Moake: Endothelial cell ADAMTS-13 and VWF: production, release, and VWF string cleavage. in Blood 2009
The levels of ADAMTS13 among neonates were higher as compared with healthy adults, despite a significant elevation of VWF (show VWF Antibodies) antigen (Ag) and Ristocetin cofactor (RiCof) noted in all neonates.
investigated the roles of ADAMTS13 and VWF (show VWF Antibodies) in thrombotic events of patients with Connective Tissue Diseases
Studied the significance of the von Willebrand factor (VWF (show VWF Antibodies))/ ADAMTS-13 ratio in advanced non-small-cell lung cancer (NSCLC). Findings suggest that the imbalance between VWF (show VWF Antibodies) secretion and ADAMTS-13 may play a role in the hypercoagulability state in advanced NSCLC, and increase of the plasma VWF (show VWF Antibodies)/ADAMTS-13 ratio may serve as an independent predictive factor for mortality in patients with advanced NSCLC.
vaso-occlusive crisis in sickle cell disease is associated with increased reactivity of VWF (show VWF Antibodies), without a pronounced ADAMTS-13 deficiency
The endogenous plasmin (show PLG Antibodies) activation alone is not sufficient to cause Thrombotic thrombocytopenic purpura (TTP), but plasmin (show PLG Antibodies) activation with ADAMTS13 deficiency might increase the risk of TTP onset.
the N-linked glycans of ADAMTS-13 play a crucial role in regulating ADAMTS-13 activity
Complex VWF (show VWF Antibodies)-ADAMTS13-mediated mechanisms disturb haemostasis in inflammatory bowel disease.
Missense variant in ADAMTS13 gene in a patient with NCIPH decreases secretion and activity of ADAMTS13 protein.
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]
Data indicate that in cultured endothelial cells, one role of endogenous ADAMTS-13 is regulation of angiogenesis, mediated through VEGF (show VEGFA Antibodies) and AKT (show AKT1 Antibodies) signaling pathway.
ADAMTS13-vWF (show VWF Antibodies) axis is partially involved in the pathophysiology of kidney ischemic reperfusion injury.
Adamts13 deficiency in obese mice promotes hepatic microthrombosis.
results suggest that ADAMTS13 controls key steps of ischemic vascular remodeling and that recombinant ADAMTS13 is a putative therapeutic avenue for promoting stroke recovery.
ADAMTS13 retards progression of diabetic nephropathy, most likely by inhibiting VWF (show VWF Antibodies)-dependent intrarenal thrombosis.
administration of ADAMTS13 5 minutes after occlusion dose-dependently dissolved these t-PA (show PLAT Antibodies)-resistant thrombi resulting in fast restoration of MCA (show RSPH1 Antibodies) patency and consequently reduced cerebral infarct sizes
Sleeping beauty transposon-mediated gene therapy achieved sustained expression of transgene ADAMTS13 and long-term prophylaxis against congenital thrombotic thrombocytopenic purpura in Adamts13(-/-) mice.
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.
Letter: deficiency of ADAMTS13 results in increased formation of venous thrombosis in mice.
ADAMTS13 substrate specificity
Data indicate that the p.D187H mutation impairs ADAMTS13 activity and secretion and may contribute to thrombotic thrombocytopenic purpura.
This gene encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motif) protein family. Members of the family share several distinct protein modules, including a propeptide region, a metalloproteinase domain, a disintegrin-like domain, and a thrombospondin type 1 (TS) motif. Individual members of this family differ in the number of C-terminal TS motifs, and some have unique C-terminal domains. The enzyme encoded by this gene is the von Willebrand Factor (vWF)-cleaving protease, which is responsible for cleaving at the site of Tyr842-Met843 of the vWF molecule. A deficiency of this enzyme is associated with thrombotic thrombocytopenic purpura. Alternative splicing of this gene generates multiple transcript variants encoding different isoforms.
ADAM metallopeptidase with thrombospondin type 1 motif, 13
, A disintegrin and metalloproteinase with thrombospondin motifs 13
, a disintegrin-like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 13
, vWF-cleaving protease
, von Willebrand factor-cleaving protease
, ADAM-TS 13
, ADAMTS13 isoform IAP-b
, vWF-CP mRNA for von Willebrand factor-cleaving
, ADAM metallopeptidase with thrombospondin type 1 motif, 13 isoform 1 preproprotein-like
, A disintegrin and metalloproteinase with thrombospondin motifs 13-like
, a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 13