ArticleBlood advances2018
Protein kinase C signaling dysfunction in von Willebrand disease (p.V1316M) type 2B platelets.
Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Novel therapies for von Willebrand disease.Blood advances · 2026Review
- Historical, current and future treatments for von Willebrand disease.Haematologica · 2026Review
- Membrane procoagulation and N‑terminomics/TAILS profiling in Montreal platelet syndrome kindred with VWF p.V1316M mutation.Communications medicine · 2023Article
- Loss of P2YJournal of thrombosis and haemostasis : JTH · 2023Article
- Efficacy of platelet-inspired hemostatic nanoparticles on bleeding in von Willebrand disease murine models.Blood · 2023Article
- The impact of aberrant von Willebrand factor-GPIbα interaction on megakaryopoiesis and platelets in humanized type 2B von Willebrand disease model mouse.Haematologica · 2022Article
- Platelet dysfunction in platelet-type von Willebrand disease due to the constitutive triggering of the Lyn-PECAM1 inhibitory pathway.Haematologica · 2022Article
- A thrombopoietin receptor agonist to rescue an unusual platelet transfusion-induced reaction in a p.V1316M-associated von Willebrand disease type 2B patient.Therapeutic advances in hematology · 2022Article
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
von Willebrand disease (VWD) type 2B is characterized by gain-of-function mutations in von Willebrand factor (VWF), enhancing its binding affinity for the platelet receptor glycoprotein (GP)Ibα. VWD type 2B patients display a bleeding tendency associated with loss of high-molecular-weight VWF multimers and variable thrombocytopenia. We recently demonstrated that a marked defect in agonist-induced activation of the small GTPase, Rap1, and integrin αIIbβ3 in VWD (p.V1316M) type 2B platelets also contributes to the bleeding tendency. Here, we investigated the molecular mechanisms underlying impaired platelet Rap1 signaling in this disease. Two distinct pathways contribute to Rap1 activation in platelets: rapid activation mediated by the calcium-sensing guanine nucleotide exchange factor CalDAG-GEF-I (CDGI) and sustained activation that is dependent on signaling by protein kinase C (PKC) and the adenosine 5'-diphosphate receptor P2Y12. To investigate which Rap1 signaling pathway is affected, we expressed VWF/p.V1316M by hydrodynamic gene transfer in wild-type and
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