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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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Submitted November 8, 2004
Accepted December 22, 2004
ADAMTS13 Turns 3
Gallia G Levy, David G Motto*, and David Ginsburg
Cell and Molecular Biology Program, University of Michigan, Ann Arbor, MI, USA
Department of Pediatrics, University of Michigan, Ann Arbor, MI, USA
Cell and Molecular Biology Program, University of Michigan, Ann Arbor, MI, USA; Departments of Internal Medicine and Human Genetics and Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, USA
* Corresponding author; email: dgmotto{at}umich.edu.
It has now been 3 years since the VWF-cleaving protease implicated in TTP pathogenesis was identified as ADAMTS13. Greater 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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