Mutations in a member of the ADAMTS gene family cause thrombotic thrombocytopenic purpura
By G. Levy, W. Nichols, E. Lian, T. Foroud, J. McClintick, B. McGee, A. Yang, D. Siemieniak, K. R. Stark, R. Gruppo and 9 more. Nature, 2001
1,769 citations recorded by the source corpus.
Subfields: Epidemiology, Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/a649971bbd52454670433dab6d5ec679b1c496eb
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Citations in the corpus
- ADAM and ADAMTS Family Proteins and Snake Venom Metalloproteinases: A Structural Overview (2016, background): “ADAMTS13 is one of the most studied ADAMTSs because of its critical involvement in a thrombotic disorder [17,18].”
- Platelet-neutrophil-interactions: linking hemostasis and inflammation. (2007, background): “vWF secreted from endothelial cells is rich in ultra large (UL) multimers and is normally cleaved by a disintegrin and metalloprotease with thrombospondin motif (ADAMTS) 13 into smaller and less active forms.(36,37) The disruption of the balance between vWF release and cleavage by ADAMTS 13 can lead”
- ADAMTS proteins in human disorders (2018, background): “Acquired thrombotic thrombocytopenic purpura (aTTP), the more common form, is an autoimmune disorder caused by antibodies to ADAMTS13 [90], whereas, congenital TTP (cTTP) is much rarer and caused by ADAMTS13 mutations [91].”
- The ADAMTS (A Disintegrin and Metalloproteinase with Thrombospondin motifs) family (2015, background): “multimers in the circulation, resulting in platelet aggregation and vessel occlusion [54].”