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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 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.
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.
The complex differential diagnosis between thrombotic thrombocytopenic purpura and the atypical hemolytic uremic syndrome: Laboratory weapons and their impact on treatment choice and monitoring.
Cugno et al., Milano, Italy. In Thromb Res, Nov 2015
TTP, inherited or autoimmune, is mainly caused by the plasma deficiency of the von Willebrand factor cleaving protease ADAMTS13, owing to gene mutations or autoantibodies.
Relevance of ADAMTS13 to liver transplantation and surgery.
Nakajima et al., Nara, Japan. In World J Hepatol, Aug 2015
A disintegrin-like and metalloproteinase with thrombospondin type-1 motifs 13 (ADAMTS13) specifically cleaves unusually-large von Willebrand factor (VWF) multimers under high shear stress, and down-regulates VWF function to form platelet thrombi.
Acquired thrombotic thrombocytopenic purpura: new therapeutic options and their optimal use.
Wu et al., Columbus, United States. In J Thromb Haemost, Jun 2015
Additionally, a recombinant ADAMTS13 protease has been developed which may be an important therapeutic option for both congenital and acquired TTP.
Life after acquired thrombotic thrombocytopenic purpura: morbidity, mortality, and risks during pregnancy.
Vesely, Oklahoma City, United States. In J Thromb Haemost, Jun 2015
Patients who have recovered from their acute episode of acquired ADAMTS13-deficient thrombotic thrombocytopenic purpura (TTP) were once thought to have complete recovery except for risk of relapse.
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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