ArticleBlood2014
Exploiting the kinetic interplay between GPIbα-VWF binding interfaces to regulate hemostasis and thrombosis.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
11 citing papers in PubMed.
- Mouse models to study von Willebrand factor in thrombosis: a scoping review.Research and practice in thrombosis and haemostasis · 2026Article
- Tissue factor, factor VIII and IX in microvesicle-induced thrombosis and tumor growth of pancreatic cancer.Thrombosis journal · 2025Article
- [Rare VPS33B gene mutation combined with GP1BA mutation causes severe decrease in plasma VWF levels: a case report and literature review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2024Review
- Autoinhibitory module underlies species difference in shear activation of von Willebrand factor.Journal of thrombosis and haemostasis : JTH · 2022Article
- The N-terminal autoinhibitory module of the A1 domain in von Willebrand factor stabilizes the mechanosensor catch bond.RSC chemical biology · 2022Article
- Biomechanical thrombosis: the dark side of force and dawn of mechano-medicine.Stroke and vascular neurology · 2020Review
- Vwf K1362A resulted in failure of protein synthesis in mice.International journal of hematology · 2018Article
- Glycoprotein Ibα inhibitor (CCP-224) prevents neutrophil-platelet aggregation in Sickle Cell Disease.Blood advances · 2017Article
- P2YJACC. Basic to translational science · 2017Article
- Transport physics and biorheology in the setting of hemostasis and thrombosis.Journal of thrombosis and haemostasis : JTH · 2016Review
- Force-induced on-rate switching and modulation by mutations in gain-of-function von Willebrand diseases.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Platelet-von Willebrand factor (VWF) interactions must be tightly regulated in order to promote effective hemostasis and prevent occlusive thrombus formation. However, it is unclear what role the inherent properties of the bond formed between the platelet receptor glycoprotein Ibα and the A1 domain of VWF play in these processes. Using VWF-A1 knock-in mice with mutations that enhance (I1309V) or disrupt (R1326H) platelet receptor glycoprotein Ibα binding, we now demonstrate that the kinetic interplay between two distinct contact surfaces influences the site and extent to which platelets bind VWF. Incorporation of R1326H mutation into the major site shortened bond lifetime, yielding defects in hemostasis and thrombosis comparable to VWF-deficient animals. Similarly, disrupting this region of contact with an allosteric inhibitor impaired human platelet accrual in damaged arterioles. In contrast, the I1309V mutation near the minor site prolonged bond lifetime, which was essential for the development of a type 2B-like VWD phenotype. However, combining the R1326H and I1309V mutations normalized both bond kinetics and the hemostatic and thrombotic properties of VWF. These findings broaden our understanding of mechanisms governing platelet-VWF interactions in health and disease, and underscore the importance of combined biophysical and genetic approaches in identifying potential therapeutic avenues for treating bleeding and thrombotic disorders.
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Registered trials
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