Adamts 13
Mostrando 13-24 de 25 artigos, teses e dissertações.
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13. Avaliação de alterações moleculares nos genes do FVW e da ADAMTS 13 e sua correlação com os niveis plasmaticos de FVIII e FVW em pacientes com trombose venenosa profunda / Molecular changes in vWF and ADAMTS 13 genes and their correlation with plasma levels of FVIII and vWF in patients with deep venous thrombosis
Níveis elevados de fator VIII (FVIII) são um fator de risco independente e prevalente para trombose venosa profunda (TVP), e tem influência do FvW. A ADAMTS13 é responsável pela modulação do tamanho molecular do FvW, clivando os multímeros de altíssimo peso molecular. Alterações moleculares no gene da ADAMTS13 têm correlação com sua atividade.
Publicado em: 2009
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14. Estudo de biomarcadores de trombose do acesso vascular em pacientes sob hemodiálise
Hemodialysis is a kind of blood filtration in which accumulated toxins and water are removed from the body. This treatment is indicated for patients in the end stage renal disease. Vascular access complications constitute about 20-25% of all hospitalizations in dialysed patients. The occurrence of thrombosis in the vascular access is a serious problem that m
Publicado em: 2009
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15. Functionally genetic thrombogenic variants related to P2Y12 platelet receptor and metaloprotease ADAMTS13 in coronary disease patients / Avaliação das variantes genéticas funcionais trombogênicas relacionadas ao receptor plaquetário P2Y12 e à metaloprotease ADAMTS13 em pacientes apresentando doença arterial coronariana
Variantes genéticas trombogênicas podem aumentar o risco de eventos adversos em pacientes com coronariopatia crônica. Estudos prévios demonstraram que o Haplótipo H2 do gene do receptor P2Y12 apresenta uma maior agregação plaquetária e está associado com a presença de isquemia arterial periférica. A metaloprotease ADAMTS13 é responsável pela cli
Publicado em: 2008
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16. The distal carboxyl-terminal domains of ADAMTS13 are required for regulation of in vivo thrombus formation
ADAMTS13 is a multidomain protease that limits platelet thrombogenesis through the cleavage of von Willebrand factor (VWF). We previously identified 2 types of mouse Adamts13 gene: the 129/Sv-strain Adamts13 gene encodes the long-form ADAMTS13 having the same domains as human ADAMTS13, whereas the C57BL/6-strain Adamts13 gene encodes the short-form ADAMTS13
American Society of Hematology.
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17. Crystal structures of the noncatalytic domains of ADAMTS13 reveal multiple discontinuous exosites for von Willebrand factor
ADAMTS13 specifically cleaves plasma von Willebrand factor (VWF) and thereby controls VWF-mediated platelet thrombus formation. Severe deficiencies in ADAMTS13 can cause life-threatening thrombotic thrombocytopenic purpura. Here, we determined 2 crystal structures of ADAMTS13-DTCS (residues 287–685), an exosite-containing human ADAMTS13 fragment, at 2.6-�
National Academy of Sciences.
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18. ADAMTS13 Bound to Endothelial Cells Exhibits Enhanced Cleavage of von Willebrand Factor*
ADAMTS13 is a plasma metalloprotease that cleaves ultralarge von Willebrand factor multimers to generate less thrombogenic fragments. Although this cleavage can occur at the surface of endothelial cells, it is currently unknown whether this process involves binding of the ADAMTS13 to the endothelial cell plasma membrane. Using different assay systems, we pre
American Society for Biochemistry and Molecular Biology.
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19. von Willebrand factor–cleaving protease ADAMTS13 reduces ischemic brain injury in experimental stroke
Stroke is a leading cause of death and disability. The only therapy available is recombinant tissue plasminogen activator, but side effects limit its use. Platelets play a crucial role during stroke, and the inflammatory reaction promotes neurodegeneration. von Willebrand factor (VWF), an adhesion molecule for platelets, is elevated in patients with acute st
American Society of Hematology.
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20. Binding of platelet glycoprotein Ibα to von Willebrand factor domain A1 stimulates the cleavage of the adjacent domain A2 by ADAMTS13
von Willebrand factor (vWF) is a multimeric plasma glycoprotein with three tandem A domains. Domains A1 and A3 bind to platelet glycoprotein Ibα (GPIbα) and collagen, respectively. Domain A2 contains the Tyr-1605–Met-1606 bond that is cleaved by the metalloprotease ADAMTS13, and this reaction inhibits platelet thrombus growth. Fluid shear stress increase
National Academy of Sciences.
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21. Leukocyte proteases cleave von Willebrand factor at or near the ADAMTS13 cleavage site
The function of von Willebrand factor (VWF) is regulated by proteolysis, which limits its multimeric size and ability to tether platelets. The importance of ADAMTS13 metalloprotease in VWF regulation is demonstrated by the association between severe deficiency of ADAMTS13 and thrombotic thrombocytopenic purpura (TTP). However, ADAMTS13 activity levels do not
American Society of Hematology.
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22. Homozygous Mutations in ADAMTS10 and ADAMTS17 Cause Lenticular Myopia, Ectopia Lentis, Glaucoma, Spherophakia, and Short Stature
Weill-Marchesani syndrome (WMS) is a well-characterized disorder in which patients develop eye and skeletal abnormalities. Autosomal-recessive and autosomal-dominant forms of WMS are caused by mutations in ADAMTS10 and FBN1 genes, respectively. Here we report on 13 patients from seven unrelated families from the Arabian Peninsula. These patients have a const
Elsevier.
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23. A new name in thrombosis, ADAMTS13
The National Academy of Sciences.
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24. Mutations and common polymorphisms in ADAMTS13 gene responsible for von Willebrand factor-cleaving protease activity
von Willebrand factor (VWF) is synthesized primarily in vascular endothelial cells and secreted into the plasma as unusually large VWF multimers. Normally, these multimers are quickly degraded into smaller forms by a plasma metalloproteinase, VWF-cleaving protease (VWF-CP). Decreases in the activity of this enzyme result in congenital and acquired thrombotic
The National Academy of Sciences.