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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 (33) and ADAMTS13 Proteins (6) and many more products for this protein.
Showing 10 out of 100 products:
Human Polyclonal ADAMTS13 Primary Antibody for EIA, IHC (p) - ABIN359601
Levy, Nichols, Lian, Foroud, McClintick, McGee, Yang, Siemieniak, Stark, Gruppo, Sarode, Shurin, Chandrasekaran, Stabler, Sabio, Bouhassira, Upshaw, Ginsburg, Tsai: Mutations in a member of the ADAMTS gene family cause thrombotic thrombocytopenic purpura. in Nature 2001
Show all 7 references for 359601
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
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Human Polyclonal ADAMTS13 Primary Antibody for ELISA, IHC - ABIN4278265
Ganburged, Suda, Saito, Yamazaki, Isokawa, Moriyama: Dilated capillaries, disorganized collagen fibers and differential gene expression in periodontal ligaments of hypomorphic fibrillin-1 mice. in Cell and tissue research 2010
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Human Polyclonal ADAMTS13 Primary Antibody for IHC (p), WB - ABIN391641
Zheng, Chung, Takayama, Majerus, Sadler, Fujikawa: Structure of von Willebrand factor-cleaving protease (ADAMTS13), a metalloprotease involved in thrombotic thrombocytopenic purpura. in The Journal of biological chemistry 2001
Show all 3 references for 391641
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 references for 251718
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
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.
findings provide further evidence on the pathophysiological role for the ADAMTS13/VWF (show VWF Antibodies) axis in atherosclerosis
both in acute and chronic cerebrovascular disease patients, ADAMTS13 levels were significantly decreased, with the lowest ADAMTS13 levels found in acute stroke patients. This difference was even more distinct when the ratio of VWF:ADAMTS13 was considered. These results demonstrate the potentially important involvement of the VWF (show VWF Antibodies)/ADAMTS13 axis in ischemic stroke.
Placental trophoblasts and villous vessel endothelial cells produce a full-length and functional ADAMTS13 protease. Placental expression of ADAMTS13 exhibits a dynamic change during pregnancy, which seems to be inhibited in late pregnancy and in patients with severe preeclampsia.
ADAMTS13 activity appears to be an independent risk factor for incident prediabetes and type 2 diabetes.
both anti-ADAMTS13 IgG antibody and ADAMTS13 antigen levels correlate with outcome in thrombotic thrombocytopenic purpura with increased cardiac and neurological involvement and increased mortality.
Low ADAMTS-13 levels correlated with high levels of NTproBNP but had no independent prognostic significance. In conclusion, high VWF:Ag levels, probably representing endothelial dysfunction, are associated with prognosis in patients with AL amyloidosis, independently of other features of the disease or cardiac biomarkers.
findings highlight the complexity of glycan modifications on ADAMTS13, which may have implications for its interaction with immune- or clearance receptors containing carbohydrate recognition domains.
ADAMTS-13 levels are decreased in plasma of AML (show RUNX1 Antibodies) patients and the level of ADAMTS-13 is related to inflammation and infection of AML (show RUNX1 Antibodies) patients. Besides, low ADAMTS-13 level is one potential risk factor for AML (show RUNX1 Antibodies)
these results demonstrate that HNPs1-3 may be potent inhibitors of ADAMTS13 activity, likely by binding to the central A2 domain of VWF (show VWF Antibodies) and physically blocking ADAMTS13 binding.
Three Single Nucleotide Variants (p.Val154Ile, p.Asp187His and p.Arg421Cys) showed reduced ex vivo and in vitro ADAMTS13 levels. However, the low frequency of these variants makes it difficult to confirm their association with Deep Vein Thrombosis.
ADAMTS13 activity and VWF:Ag levels are both associated with an increased risk of all-cause and cardiovascular mortality.
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
, ADAM metallopeptidase with thrombospondin type 1 motif, 13 isoform 1 preproprotein-like
, A disintegrin and metalloproteinase with thrombospondin motifs 13-like
, ADAM metallopeptidase with thrombospondin type 1 motif, 12
, A disintegrin and metalloproteinase with thrombospondin motifs 12
, A disintegrin and metalloproteinase with thrombospondin motifs 13
, ADAM-TS 13
, ADAMTS13 isoform IAP-b
, a disintegrin-like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 13
, vWF-CP mRNA for von Willebrand factor-cleaving
, vWF-cleaving protease
, von Willebrand factor-cleaving protease
, a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 13