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Literature summary for 3.4.24.87 extracted from

  • Zhou, W.; Dong, L.; Ginsburg, D.; Bouhassira, E.E.; Tsai, H.M.
    Enzymatically active ADAMTS13 variants are not inhibited by anti-ADAMTS13 autoantibodies: a novel therapeutic strategy? (2005), J. Biol. Chem., 280, 39934-39941.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine in order to develop new strategies for improving the diagnosis and treatment of thrombotic thrombocytopenic purpura, this study systemically analyzed a series of ADAMTS13 mutant proteins to identify variant forms that are proteolytically active and yet resistant to suppression by inhibitory antibodies. A deficiency ofADAMTS13, due to mutations in the ADAMTS13 gene or the presence of antibodies that inhibit the activity of the protease,causes thrombotic thrombocytopenic purpura. Plasma therapy, the conventional therapy for TTP, may cause serious adverse reactions and is ineffective in some patients Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q76LX8 ADAMTS-13 precursor
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
von Willebrand factor + H2O
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Homo sapiens ?
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?