Zobrazeno 1 - 10
of 18
pro vyhledávání: '"Kate Sponagle"'
Autor:
Robert R. Montgomery, Boonchai Boonyawat, Kate Sponagle, Laura L. Swystun, Paula D. James, Colleen Notley, Natalia Rydz, David Lillicrap, Andrew D. Paterson, J. Jacob Riches
Publikováno v:
Blood
Genetic variation in or near the C-type lectin domain family 4 member M (CLEC4M) has been associated with plasma levels of von Willebrand factor (VWF) in healthy individuals. CLEC4M is a lectin receptor with a polymorphic extracellular neck region po
Autor:
Andrea Bryant, Sandra L. Haberichter, Mia Golder, Kate Sponagle, Cynthia M. Pruss, Kimberly Laverty, Erin Burnett, Colleen Notley, Carol Hegadorn, David Lillicrap, Aly S. Dhala
Publikováno v:
Blood. 117:4358-4366
Type 1 VWD is the mild to moderate reduction of VWF levels. This study examined the mechanisms underlying 2 common type 1 VWD mutations, the severe R1205H and more moderate Y1584C. In vitro biosynthesis was reduced for both mutations in human and mou
Autor:
Kimberly Laverty, Kate Sponagle, David Lillicrap, Mia Golder, Cynthia M. Pruss, Jeffrey Mewburn, Carol Hegadorn
Publikováno v:
Blood. 115:4862-4869
Type 2B von Willebrand disease (2B VWD) results from von Willebrand factor (VWF) A1 mutations that enhance VWF-GPIbα binding. These “gain of function” mutations lead to an increased affinity of the mutant VWF for platelets and the binding of mut
Autor:
Kate Sponagle, Jesse D. Lai, Christine Hough, Birgit M. Reipert, Paul Moorehead, Katharina Nora Steinitz, David Lillicrap
Publikováno v:
Blood. 127(26)
Inflammatory signals such as pathogen- and danger-associated molecular patterns have been hypothesized as risk factors for the initiation of the anti-factor VIII (FVIII) immune response seen in 25% to 30% of patients with severe hemophilia A (HA). In
Autor:
Barbara Vidal, Yasuaki Shida, Kate Sponagle, David Lillicrap, Ozge Danisment, Carol Hegadorn, Jeffrey Mewburn, David Stegner, Cynthia M. Pruss, Christine Brown, Bredon Crawford, Natalia Rydz, Bernhard Nieswandt
Publikováno v:
Blood. 124(11)
Rare missense mutations in the von Willebrand factor (VWF) A3 domain that disrupt collagen binding have been found in patients with a mild bleeding phenotype. However, the analysis of these aberrant VWF-collagen interactions has been limited. Here, w
Autor:
David Lillicrap, Christine Hough, Barbara Vidal, Paul Moorehead, Maria T. Georgescu, Alice S. van Velzen, Birgit M. Reipert, Kate Sponagle, Katharina Nora Steinitz
Publikováno v:
Blood. 124:1489-1489
Background For persons with severe hemophilia A receiving exogenous factor VIII (FVIII) replacement therapy, antibodies that interfere with the coagulant function of FVIII (inhibitors) are the most severe complication of treatment. Although avoidance
Autor:
Jesse D. Lai, Kate Sponagle, Christine Hough, Birgit M. Reipert, Katharina Nora Steinitz, David Lillicrap, Paul Moorehead
Publikováno v:
Blood. 124:1501-1501
Introduction: The etiology of inhibitory factor VIII (FVIII) antibodies in 25-30% of hemophilia A (HA) patients remains poorly understood. It is possible that concurrent exposure to inflammatory stimuli, or ‘danger signals’, with FVIII increases
Characterization of Type 2N Von Willebrand Disease Mutations Using Ιn Vitro and Ιn Vivo Mouse Models
Autor:
Kate Sponagle, Christine Brown, Mia Golder, Colleen Notley, Ilinca Georgescu, Laura L. Swystun, Meghan Deforest, David Lillicrap
Publikováno v:
Blood. 124:471-471
Introduction: Von Willebrand factor (VWF) is a multimeric glycoprotein that serves as the carrier for the essential coagulation cofactor, factor VIII (FVIII). Both plasma levels of VWF and its FVIII-binding ability can influence plasma levels of FVII
Autor:
David Lillicrap, Kate Sponagle, Laura L. Swystun, Jeffrey Mewburn, Silvia Albánez, Alison Michels
Publikováno v:
Blood. 124:2768-2768
Thrombosis is the leading cause of mortality worldwide and can result from uncontrolled immune activation in inflammatory conditions. Von Willebrand factor (VWF) is an acute phase glycoprotein that mediates primary hemostasis by binding to platelets.
Autor:
Paul Moorehead, Birgit M. Reipert, David Lillicrap, Christine Hough, Maria T. Georgescu, Kate Sponagle
Publikováno v:
Blood. 124:237-237
Background: The most severe complication of hemophilia A (HA) treatment is the development of inhibitory antibodies (inhibitors) to factor VIII (FVIII). The presence of immunological ‘danger signals’ during initial exposure to FVIII may increase