ArticleThe Journal of biological chemistry2003
Cleavage of the ADAMTS13 propeptide is not required for protease activity.
Article in The Journal of biological chemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 122 citations in OpenAlex.
- Hyperadhesive von Willebrand Factor Contributes to Pathogenesis of Preeclampsia.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Open or closed? Understanding the molecular mechanisms and clinical implications of ADAMTS13's conformation.HemaSphere · 2025Review
- Autoantibodies to ADAMTS13 in human immunodeficiency virus-associated thrombotic thrombocytopenic purpura.Vox sanguinis · 2024Article
- Phylogenetic inference of the emergence of sequence modules and protein-protein interactions in the ADAMTS-TSL family.PLoS computational biology · 2023Article
- ADAMTS13 Biomarkers in Management of Immune Thrombotic Thrombocytopenic Purpura.Archives of pathology & laboratory medicine · 2023Review
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- ADAMTS Proteins and Vascular Remodeling in Aortic Aneurysms.Biomolecules · 2021Review
- Regulation of ADAMTS Proteases.Frontiers in molecular biosciences · 2021Review
- Pathologic Shear and Elongation Rates Do Not Cause Cleavage of Von Willebrand Factor by ADAMTS13 in a Purified System.Cellular and molecular bioengineering · 2020Article
- Turbulent Flow Promotes Cleavage of VWF (von Willebrand Factor) by ADAMTS13 (A Disintegrin and Metalloproteinase With a Thrombospondin Type-1 Motif, Member 13).Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Crystal structure and substrate-induced activation of ADAMTS13.Nature communications · 2019Article
- A Disintegrin and Metalloproteinase (ADAM) and ADAM with thrombospondin motifs (ADAMTS) family in vascular biology and disease.Biochemical pharmacology · 2019Review
- Article
- A Review of Integrin-Mediated Endothelial Cell Phenotype in the Design of Cardiovascular Devices.Annals of biomedical engineering · 2019Review
- Role of calcium in regulating the intra- and extracellular cleavage of von Willebrand factor by the protease ADAMTS13.Blood advances · 2017Article
- Unusual life cycle and impact on microfibril assembly of ADAMTS17, a secreted metalloprotease mutated in genetic eye disease.Scientific reports · 2017Article
- Vascular proteomics in metabolic and cardiovascular diseases.Journal of internal medicine · 2016Review
- Conformational quiescence of ADAMTS-13 prevents proteolytic promiscuity.Journal of thrombosis and haemostasis : JTH · 2016Article
- ADAM and ADAMTS Family Proteins and Snake Venom Metalloproteinases: A Structural Overview.Toxins · 2016Review
- ADAMTS13 and von Willebrand factor interactions.Current opinion in hematology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
ADAMTS13 belongs to the "a disintegrin and metalloprotease with thrombospondin repeats" family, and cleaves von Willebrand factor multimers into smaller forms. For several related proteases, normal folding and enzymatic latency depend on an NH2-terminal propeptide that is removed by proteolytic processing during biosynthesis. However, the ADAMTS13 propeptide is unusually short and poorly conserved, suggesting it may not perform these functions. ADAMTS13 was secreted from transfected HeLa cells with a half-time of 7 h and the rate-limiting step was exported from the endoplasmic reticulum. Deletion of the propeptide did not impair the secretion of active ADAMTS13, indicating that the propeptide is dispensable for folding. Furin was shown to be sufficient for ADAMTS13 propeptide processing in two ways. First, mutation of the furin consensus recognition site prevented propeptide cleavage in HeLa cells and resulted in secretion of pro-ADAMTS13. Second, furin-deficient LoVo cells secreted ADAMTS13 with the propeptide intact, and cotransfection with furin restored propeptide cleavage. In both cell lines, secreted pro-ADAMTS13 had normal proteolytic activity toward von Willebrand factor. In cells coexpressing both ADAMTS13 and von Willebrand factor, pro-ADAMTS13 cleaved pro-von Willebrand factor intracellularly. Therefore, the ADAMTS13 propeptide is not required for folding or secretion, and does not perform the common function of maintaining enzyme latency.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.