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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

ADAM metallopeptidase with thrombospondin type 1 motif, 13

Top mentioned proteins: von Willebrand factor, metalloprotease, thrombospondin-1, HAD, CAN
Papers on ADAMTS13
Rituximab-refractory thrombotic thrombocytopenic purpura responsive to intravenous but not subcutaneous bortezomib.
Wang et al., Buffalo, United States. In Transfusion, Feb 2016
BACKGROUND: Thrombotic thrombocytopenic purpura (TTP) is often characterized by formation of antibodies against a disintegrin and metalloprotease with thrombospondin repeat, member 13 (ADAMTS13).
N-linked glycan stabilisation of the VWF A2 domain.
Lane et al., London, United Kingdom. In Blood, Feb 2016
UNASSIGNED: Shear forces in the blood trigger a conformational transition in the VWF A2 domain, from its native folded to an unfolded state, in which the cryptic scissile bond (Y1505-M1606) is exposed and can then be proteolysed by ADAMTS13.
Plasma ADAMTS13, von Willebrand Factor (VWF), and VWF Propeptide Profiles in Patients With Connective Tissue Diseases and Antiphospholipid Syndrome.
Mizutani et al., Tsu, Japan. In Clin Appl Thromb Hemost, Feb 2016
ADAMTS13 and von Willebrand factor (VWF) are closely related to the onset of TTP.
Plasma ADAMTS-13 protein is not associated with portal hypertension or hemodynamic changes in patients with cirrhosis.
Møller et al., Hvidovre, Denmark. In Dig Liver Dis, Jan 2016
BACKGROUND: Activated hepatic stellate cells synthesize the matrix metalloprotease ADAMTS13, which may be involved in the development of liver cirrhosis and portal hypertension.
ADAMTS13 and anti-ADAMTS13 autoantibodies in thrombotic thrombocytopenic purpura - current perspectives and new treatment strategies.
Vanhoorelbeke et al., Kortrijk, Belgium. In Expert Rev Hematol, Jan 2016
UNASSIGNED: A deficiency in ADAMTS13 (A Disintegrin And Metalloprotease with ThromboSpondin type-1 repeats, member 13) is associated with thrombotic thrombocytopenic purpura (TTP).
Treatment of thrombotic thrombocytopenic purpura beyond therapeutic plasma exchange.
French Reference Center for Thrombotic Microangiopathies et al., Paris, France. In Hematology Am Soc Hematol Educ Program, Jan 2016
Daily therapeutic plasma exchange (TPE) transformed the historically fatal prognosis of acquired, anti-ADAMTS13 antibody-mediated thrombotic thrombocytopenic purpura (TTP), leading to the current overall survival rates of 80%-85%.
Pregnancy associated thrombotic thrombocytopenic purpura: Practical issues for patient management.
De Angelis et al., Udine, Italy. In Transfus Apher Sci, Dec 2015
Our understanding of the pathophysiology of TTP has allowed ADAMTS13 testing to have a central role in confirming the clinical diagnosis but the main limitation is that an ADAMTS13 assay is not available in "real time".
Association of Haemostatic and Inflammatory Biomarkers with Nephropathy in Type 1 Diabetes Mellitus.
Fernandes et al., Divinópolis, Brazil. In J Diabetes Res, Dec 2015
VWF, ADAMTS13 antigen, and D-Dimer plasma levels were determined by enzyme-linked immunosorbent assay and ADAMTS13 activity was assessed by fluorescence resonance energy transfer assay.
Keeping von Willebrand Factor under Control: Alternatives for ADAMTS13.
Maas et al., Kortrijk, Belgium. In Semin Thromb Hemost, Dec 2015
ADAMTS13 is the key protease that regulates the multimeric state of VWF.
Role of fluid shear stress in regulating VWF structure, function and related blood disorders.
Neelamegham et al., Buffalo, United States. In Biorheology, Dec 2015
Once in blood, the protein multimer distribution is dynamically regulated by fluid shear stress which has two opposing effects: it promotes the aggregation or self-association of multiple VWF units, and it simultaneously reduces multimer size by facilitating the force-dependent cleavage of the protein by various proteases, most notably ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type repeats, motif 1 type 13).
miR-525-5p inhibits ADAMTS13 and is correlated with Ischemia/reperfusion injury-induced neuronal cell death.
Wu et al., Changchun, China. In Int J Clin Exp Med, 2014
databases, we identified miR-525-5p as a possible regulator of the ADAMTS13.
Increased expression of ADAMTS13 mRNA correlates with ischemic cerebrovascular disease in systemic lupus erythematosus patients.
Reed et al., Rochester, United States. In Sage Open Med, 2012
OBJECTIVE: We investigated ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type 1 motif, member 13) messenger RNA levels as a biomarker of disease features in systemic lupus erythematosus.
ADAMTS-13 is produced by glial cells and upregulated after spinal cord injury.
Kadomatsu et al., Nagoya, Japan. In Neurosci Lett, 2012
Found that ADAMTS-13 mRNA was expressed in cultured astrocytes and microglia but not in neurons, the expression of ADAMTS-13 was significantly increased in the rat spinal cord after injury.
[Induction of expression of von Willebrand factor cleaving protease of rat aortic endothelial cell by lipopolysaccharide challenge].
Li et al., China. In Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 2011
The expression of ADAMTS-13 mRNA and protein are decreased after LPS challenge in rat aortic endothelial cells.
Increased production of ADAMTS13 in hepatic stellate cells contributes to enhanced plasma ADAMTS13 activity in rat models of cholestasis and steatohepatitis.
Yatomi et al., Tokyo, Japan. In Thromb Haemost, 2009
increased plasma ADAMTS13 activity in cholestasis and steatohepatitis in may be due to enhanced ADAMTS13 production in the liver, suggesting a role of hepatic stellate cells in the regulation of plasma ADAMTS13 activity
Mechanoenzymatic cleavage of the ultralarge vascular protein von Willebrand factor.
Springer et al., Boston, United States. In Science, 2009
Von Willebrand factor (VWF) is secreted as ultralarge multimers that are cleaved in the A2 domain by the metalloprotease ADAMTS13 to give smaller multimers.
Inflammatory cytokines inhibit ADAMTS13 synthesis in hepatic stellate cells and endothelial cells.
Zheng et al., In J Thromb Haemost, 2008
certain inflammatory cytokines selectively inhibit ADAMTS13 synthesis without triggering release of its known substrate, vWF.
Pathogenesis of thrombotic microangiopathies.
Sadler et al., Philadelphia, United States. In Annu Rev Pathol, 2007
The congenital and idiopathic TTP syndromes are caused primarily by deficiency of ADAMTS13, owing to mutations in the ADAMTS13 gene or autoantibodies that inhibit ADAMTS13 activity.
Hepatic stellate cell damage may lead to decreased plasma ADAMTS13 activity in rats.
Yatomi et al., Tokyo, Japan. In Febs Lett, 2007
These results suggest that HSC may be involved in the regulation of plasma ADAMTS13 activity.
Mutations in a member of the ADAMTS gene family cause thrombotic thrombocytopenic purpura.
Tsai et al., Ann Arbor, United States. In Nature, 2001
A predicted gene in the identified interval corresponds to a segment of a much larger transcript, identifying a new member of the ADAMTS family of zinc metalloproteinase genes (ADAMTS13).
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