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ADAMTS13 encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motif) protein family. Additionally we are shipping ADAMTS13 Kits (38) and ADAMTS13 Proteins (6) and many more products for this protein.
Showing 10 out of 100 products:
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
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 haplotype had an independent protective effect on CAD (show CAD Antibodies) and genetic variation of vWF (show VWF Antibodies) V1565L polymorphism modulates ADAMTS13 activity.
The relative deficiency of plasma ADAMTS13 activity in subarachnoid haemorrhage patients may associate with worse outcome.
Low ADAMTS13 was associated with increased mortality in patients with severe sepsis and septic shock and was comparable to APACHE II scores for predicting mortality.
These observations support the hypothesis that a significantly reduced ADAMTS13/VWF (show VWF Antibodies) ratio in the coronary artery flow plays a pathogenic role in acute coronary syndromes (ACS (show PLA2G15 Antibodies)) and suggest that transition from laminar to turbulent flow at sites of coronary stenosis further enhances VWF (show VWF Antibodies) activation and deposition.
Low ADAMTS-13 activity is associated with an increased risk of coronary heart disease in the elderly, independently of VWF (show VWF Antibodies) and established cardiovascular risk factors
As folding stability was progressively disrupted, proteolysis by ADAMTS13 increased. Due to the range of folding stabilities and wide distribution of VWF (show VWF Antibodies) A2 domain mutations studied, we conclude that these mutations disrupt regulated folding of the VWF (show VWF Antibodies) A2 domain
The 'closed' conformation of ADAMTS-13 restricts its specificity and protects against fibrinogenolysis
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.
Data show that metalloendopeptidase (show THOP1 Antibodies) ADAMTS13 does not directly promote development of adipose tissue.
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