ArticleHaematologica2022
The GPIbα intracellular tail - role in transducing VWF- and collagen/GPVI-mediated signaling.
Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
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- Harnessing flavonoids as innovative agents for the modulation of platelet activation and thrombotic disorders.Molecular biology reports · 2026Review
- Platelet-Collagen Interactions in Hemostatic Mechanisms.Advanced healthcare materials · 2026Review
- Inhibitory effects of ethanol on pathological high shear stress-induced platelet adhesion and aggregation: a microfluidic chip model study.Thrombosis journal · 2026Article
- Platelet-membrane-coated nanoparticles enable safe and targeted thrombolysis with preserved neurovascular integrity.Frontiers in pharmacology · 2026Article
- Direct Binding of Lyn to GPIbβ Transmits 2-Way GPIb-IX Signaling to Stimulate Platelet Activation and VWF Binding.Circulation research · 2025Article
- Low-Molecular-Weight Fucoidan Inhibits Thromboinflammation and Ameliorates Deep Vein Thrombosis via Targeting S100A8/A9.Marine drugs · 2025Article
- Calcium levels modulate platelet function, platelet-cancer cell interaction, and cancer cell invasion.Scientific reports · 2025Article
- Is GPIbα really a master regulator of platelet activation?Blood advances · 2025Article
- Oxymatrine, a novel TLR2 agonist, promotes megakaryopoiesis and thrombopoiesis through the STING/NF-κB pathway.Journal of pharmaceutical analysis · 2025Article
- Platelet Glycoprotein Ibα Cytoplasmic Tail Exacerbates Thrombosis During Bacterial Sepsis.International journal of molecular sciences · 2024Article
- Essential role of glycoprotein Ibα in platelet activation.Blood advances · 2024Article
- Is glycoprotein VI involved in contractual negotiations?Research and practice in thrombosis and haemostasis · 2024Article
- Microvascular Thrombosis as a Critical Factor in Severe COVID-19.International journal of molecular sciences · 2023Article
- Platelet-Neutrophil Crosstalk in Thrombosis.International journal of molecular sciences · 2023Review
- Analysis of thrombogenicity under flow reveals new insights into the prothrombotic state of patients with post-COVID syndrome.Journal of thrombosis and haemostasis : JTH · 2023Article
- Role of BMP-7 on biological parameters osseointegration of dental implants: Preliminary results of a preclinical study.Frontiers in bioengineering and biotechnology · 2023Article
- Targeting TLR2/Rac1/cdc42/JNK Pathway to Reveal That Ruxolitinib Promotes Thrombocytopoiesis.International journal of molecular sciences · 2022Article
- Signaling mechanisms of the platelet glycoprotein Ib-IX complex.Platelets · 2022Review
- Neuroprotective Effects of Quercetin on Ischemic Stroke: A Literature Review.Frontiers in pharmacology · 2022Review
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The GPIbT-VWF A1 domain interaction is essential for platelet tethering under high shear. Synergy between GPIbα and GPVI signaling machineries has been suggested previously, however its molecular mechanism remains unclear. We generated a novel GPIbα transgenic mouse (GpIbαΔsig/Δsig) by CRISPR-Cas9 technology to delete the last 24 residues of the GPIbα intracellular tail that harbors the 14-3-3 and phosphoinositide-3 kinase binding sites. GPIbαΔsig/Δsig platelets bound VWF normally under flow. However, they formed fewer filopodia on VWF/botrocetin in the presence of a oIIbI3 blocker, demonstrating that despite normal ligand binding, VWF-dependent signaling is diminished. Activation of GpIbαΔsig/Δsig platelets with ADP and thrombin was normal, but GpIbαΔsig/Δsig platelets stimulated with collagen-related-peptide (CRP) exhibited markedly decreased P-selectin exposure and eIIbI3 activation, suggesting a role for the GpIbaaintracellular tail in GPVI-mediated signaling. Consistent with this, while haemostasis was normal in GPIbαΔsig/Δsig mice, diminished tyrosine-phosphorylation, (particularly pSYK) was detected in CRP-stimulated GpIbαΔsig/Δsig platelets as well as reduced platelet spreading on CRP. Platelet responses to rhodocytin were also affected in GpIbαΔsig/Δsig platelets but to a lesser extent than those with CRP. GpIbαΔsig/Δsig platelets formed smaller aggregates than wild-type platelets on collagen-coated microchannels at low, medium and high shear. In response to both VWF and collagen binding, flow assays performed with plasma-free blood or in the presence of bIIbI3- or GPVI-blockers suggested reduced bIIbI3 activation contributes to the phenotype of the GpIbαΔsig/Δsig platelets. Together, these results reveal a new role for the intracellular tail of GPIbiiin transducing both VWF-GPIbGGand collagen-GPVI signaling events in platelets.
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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.