ArticleRSC chemical biology2022
The N-terminal autoinhibitory module of the A1 domain in von Willebrand factor stabilizes the mechanosensor catch bond.
Article in RSC chemical biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Flow molecular dynamics simulations reveal mechano-presentation of von Willebrand factor through glycan-modulated autoinhibitory modules.APL bioengineering · 2026Article
- Mechanoimmunology: past, present, and future perspectives.Mechanobiology in medicine · 2026Review
- Vicinal disulfide bond modulates A1-GPIbα interaction by altering the force-induced conformational changes of A2 domain.Communications biology · 2025Article
- Microscale geometrical modulation of PIEZO1 mediated mechanosensing through cytoskeletal redistribution.Nature communications · 2024Article
- Conformational activation and inhibition of von Willebrand factor by targeting its autoinhibitory module.Blood · 2024Article
- Protein disulfide isomerase cleaves allosteric disulfides in histidine-rich glycoprotein to regulate thrombosis.Nature communications · 2024Article
- Molecular mechanisms of catch bonds and their implications for platelet hemostasis.Biophysical reviews · 2023Review
- Biomembrane force probe (BFP): Design, advancements, and recent applications to live-cell mechanobiology.Exploration (Beijing, China) · 2023Review
- Biomechanical activation of blood platelets via adhesion to von Willebrand factor studied with mesoscopic simulations.Biomechanics and modeling in mechanobiology · 2023Article
- Type 2B von Willebrand disease mutations differentially perturb autoinhibition of the A1 domain.Blood · 2023Article
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The von Willebrand factor (VWF), by interacting with the circulatory system and platelets, harnesses hemodynamic forces to form hemostatic plugs or occlusive thrombi. The autoinhibitory modules (AIMs) flanking the VWF-A1 domain were found to contribute to its biomechanical activation. However, how AIM sequences regulate the VWF-A1 binding behavior is controversial and incompletely understood as their structures are currently unsolvable by crystallography. To address this, we first performed molecular dynamics simulations to predict the N-terminal AIM (N-AIM; residues Q1238-E1260) structure. Excitingly, we found that N-AIM could cooperate with C-AIM to form a joint Rotini-like structure, thereby partially autoinhibiting the VWF-A1-GPIbα interaction. Furthermore, we used biomembrane force probe (BFP) assays to experimentally demonstrate that the VWF-A1 containing long N-AIM sequence (1238-A1) exhibited catch-bond behavior as the force first decelerated (catch) and then accelerated (slip) the dissociation. Conversely, VWF-A1 with short N-AIM (1261-A1) displayed bi-variable behaviors with either catch (1261
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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.