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Blood, 1 July 2005, Vol. 106, No. 1, pp. 11-17.
Prepublished online as a Blood First Edition Paper on March 17, 2005; DOI 10.1182/blood-2004-10-4097.
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REVIEW IN TRANSLATIONAL HEMATOLOGY
ADAMTS13 turns 3
Gallia G. Levy,
David G. Motto, and
David Ginsburg
From the Cell and Molecular Biology Program and the Department of Pediatrics, University of Michigan, Ann Arbor; the Department of Internal Medicine, Howard Hughes Medical Institute, University of Michigan, Ann Arbor; and the Department of Human Genetics, Howard Hughes Medical Institute, University of Michigan, Ann Arbor.
Abstract
It has now been 3 years since the von Willebrand factor (VWF)–cleaving protease implicated in thrombocytopenic purpura (TTP) pathogenesis was identified as ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type 1 motif 13). More than 50 ADAMTS13 mutations resulting in familial TTP have been reported. Considerable progress has also been realized toward understanding the role of ADAMTS13 in normal hemostasis, as well as the mechanisms by which ADAMTS13 deficiency contributes to TTP pathogenesis. Measurement of ADAMTS13 activity in TTP and other pathologic conditions also remains a focus of a substantial clinical research effort. Building on these studies, continued investigation of ADAMTS13 and VWF holds considerable promise for advancing the understanding of TTP pathogenesis and should lead to improved diagnosis and treatment for this important hematologic disease.
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