Associated Papers
Global prevalence of hereditary thrombotic thrombocytopenic purpura determined by genetic analysis.
Seidizadeh O et al.
Blood Advances, 2024
38935915 (PubMed )
Supplement: BLOODA_ADV-2024-013421-mmc1.pdf
Carriers of ADAMTS13 Rare Variants Are at High Risk of Life-Threatening COVID-19.
Zguro K et al.
Viruses, 2022
The global carrier frequency and genetic prevalence of Upshaw-Schulman syndrome.
Zhao T et al.
Bmc Genomic Data, 2021
34789164 (PubMed )
Supplement: 12863_2021_1010_MOESM10_ESM.xlsx › HGMD
Proteolysis of Von Willebrand Factor Influences Inflammatory Endothelial Activation and Vascular Compliance in Atherosclerosis.
Ozawa K et al.
Jacc. Basic to Translational Science, 2020
Upshaw-Schulman syndrome-associated ADAMTS13 variants possess proteolytic activity at the surface of endothelial cells and in simulated circulation.
Letzer A et al.
Plos One, 2020
Pathophysiology of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome.
Kremer Hovinga JA et al.
Journal of Thrombosis and Haemostasis : Jth, 2018
Genetic and Functional Characterization of ADAMTS13 Variants in a Patient Cohort with Upshaw-Schulman Syndrome Investigated in Germany.
Hassenpflug WA et al.
Thrombosis and Haemostasis, 2018
Interaction between Multimeric von Willebrand Factor and Complement: A Fresh Look to the Pathophysiology of Microvascular Thrombosis.
Bettoni S et al.
Journal of Immunology (baltimore, Md. : 1950), 2017
ADAMTS13 Secretion and Residual Activity among Patients with Congenital Thrombotic Thrombocytopenic Purpura with and without Renal Impairment.
Rurali E et al.
Clinical Journal of the American Society of Nephrology : Cjasn, 2015
Multiple in silico tools predict phenotypic manifestations in congenital thrombotic thrombocytopenic purpura.
Hing ZA et al.
British Journal of Haematology, 2013
Residual plasmatic activity of ADAMTS13 is correlated with phenotype severity in congenital thrombotic thrombocytopenic purpura.
Lotta LA et al.
Blood, 2012
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