ArticleNature communications2021
Activation of von Willebrand factor via mechanical unfolding of its discontinuous autoinhibitory module.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- P2Y12-P-selectin-mediated platelet activation in a murine model of dengue-associated thrombocytopenia.EBioMedicine · 2026Article
- Von Willebrand factor A2 domain inhibits A1-DNA binding while preserving A1-platelet interaction under flow: evidence from recombinant domain constructs.Research and practice in thrombosis and haemostasis · 2026Article
- Platelet-Collagen Interactions in Hemostatic Mechanisms.Advanced healthcare materials · 2026Review
- Identification of missense variants in the C-domains of von Willebrand factor that cause gain-of-function-like activity.Blood advances · 2026Article
- Flow molecular dynamics simulations reveal mechano-presentation of von Willebrand factor through glycan-modulated autoinhibitory modules.APL bioengineering · 2026Article
- Von Willebrand disease: A century of progress.Research and practice in thrombosis and haemostasis · 2026Review
- Multimodal characterization of flow-induced thrombus initiation and growth in extracorporeal membrane oxygenation.Scientific reports · 2026Article
- Blood Mechanical Intelligence: From Force Sensing to Precision Mechanomedicine.Research (Washington, D.C.) · 2026Review
- Structure and multiple functions of von Willebrand factor.Haematologica · 2026Review
- Cellular and molecular mechanisms of thrombosis and thrombus-targeted thrombolytic strategies.Materials today. Bio · 2025Review
- Hydrodynamic-derived centrifugal blood pump design for stable-low-flow-rate rate performance: from surface to structure.Bioactive materials · 2025Article
- Vicinal disulfide bond modulates A1-GPIbα interaction by altering the force-induced conformational changes of A2 domain.Communications biology · 2025Article
- Review
- Open or closed? Understanding the molecular mechanisms and clinical implications of ADAMTS13's conformation.HemaSphere · 2025Review
- Dynamics of a von Willebrand Factor A1 Autoinhibitory Module with O-Linked Glycans and Its Roles in Regulation of GPIbα Binding.The journal of physical chemistry. B · 2025Article
- FRET Visualization of High Mechanosensation of von Willebrand Factor to Hydrodynamic Force.Biosensors · 2025Article
- A mutant complement factor H (W1183R) enhances proteolytic cleavage of von Willebrand factor by ADAMTS-13 under shear.Journal of thrombosis and haemostasis : JTH · 2025Article
- The Role of the VWF/ADAMTS13 Axis in the Thromboinflammatory Response in Ischemic Stroke After SARS-CoV2 Infection.Brain and behavior · 2025Article
- A Systematic Review of risk factors for major adverse cardiovascular events in patients with coronary heart disease who underwent percutaneous coronary intervention.Frontiers in physiology · 2025Article
- Discovery of nanobodies: a comprehensive review of their applications and potential over the past five years.Journal of nanobiotechnology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Von Willebrand factor (VWF) activates in response to shear flow to initiate hemostasis, while aberrant activation could lead to thrombosis. Above a critical shear force, the A1 domain of VWF becomes activated and captures platelets via the GPIb-IX complex. Here we show that the shear-responsive element controlling VWF activation resides in the discontinuous autoinhibitory module (AIM) flanking A1. Application of tensile force in a single-molecule setting induces cooperative unfolding of the AIM to expose A1. The AIM-unfolding force is lowered by truncating either N- or C-terminal AIM region, type 2B VWD mutations, or binding of a ristocetin-mimicking monoclonal antibody, all of which could activate A1. Furthermore, the AIM is mechanically stabilized by the nanobody that comprises caplacizumab, the only FDA-approved anti-thrombotic drug to-date that targets VWF. Thus, the AIM is a mechano-regulator of VWF activity. Its conformational dynamics may define the extent of VWF autoinhibition and subsequent activation under force.
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Registered trials
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.