ArticleThe Biochemical journal1995
Integrin alpha 2 beta 1-independent activation of platelets by simple collagen-like peptides: collagen tertiary (triple-helical) and quaternary (polymeric) structures are sufficient alone for alpha 2 beta 1-independent platelet reactivity.
Article in The Biochemical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
80 citing papers in PubMed, 318 citations in OpenAlex.
- Constitutive dimerization of glycoprotein VI (GPVI) in resting platelets is essential for binding to collagen and activation in flowing blood.The Journal of biological chemistry · 2012Trial
- Trial
- High Prevalence of Acquired Platelet Secretion Defects in Multiple Myeloma.Hamostaseologie · 2026Article
- A monoclonal antibody to platelet αIIbβ3 that inhibits protein disulfide isomerase binding and platelet aggregation.Blood advances · 2026Article
- Platelet Membrane Receptors and Signalling Pathways.Handbook of experimental pharmacology · 2026Review
- Triple Helical-Peptides: Collagen-Mimicking Tools for Tissue Engineering.Methods in molecular biology (Clifton, N.J.) · 2026Article
- A minimum valency of 4 is required for robust activation of platelets in flow cytometry by multivalent nanobodies to Glycoprotein VI, C-type lectin-like receptor 2 and Platelet Endothelial Aggregation Receptor 1.Research and practice in thrombosis and haemostasis · 2025Article
- GPVI inhibition: Advancing antithrombotic therapy in cardiovascular disease.European heart journal. Cardiovascular pharmacotherapy · 2024Review
- Genetically engineered transfusable platelets using mRNA lipid nanoparticles.Science advances · 2023Article
- PACSIN2 regulates platelet integrin β1 hemostatic function.Journal of thrombosis and haemostasis : JTH · 2023Article
- Article
- Minimal Collagen-Binding Epitope of Glycoprotein VI in Human and Mouse Platelets.Biomedicines · 2023Article
- Rac Inhibition Causes Impaired GPVI Signalling in Human Platelets through GPVI Shedding and Reduction in PLCγ2 Phosphorylation.International journal of molecular sciences · 2022Article
- Mechanisms Underlying Dichotomous Procoagulant COAT Platelet Generation-A Conceptual Review Summarizing Current Knowledge.International journal of molecular sciences · 2022Review
- Platelet surface receptor glycoprotein VI-dimer is overexpressed in stroke: The Glycoprotein VI in Stroke (GYPSIE) study results.PloS one · 2022Article
- mTOR regulates GPVI-mediated platelet activation.Journal of translational medicine · 2021Article
- Protein Disulphide Isomerase and NADPH Oxidase 1 Cooperate to Control Platelet Function and Are Associated with Cardiometabolic Disease Risk Factors.Antioxidants (Basel, Switzerland) · 2021Article
- Multimerin 1 supports platelet function in vivo and binds to specific GPAGPOGPX motifs in fibrillar collagens that enhance platelet adhesion.Journal of thrombosis and haemostasis : JTH · 2021Article
- Ethaninidothioic acid (R5421) is not a selective inhibitor of platelet phospholipid scramblase activity.British journal of pharmacology · 2020Article
- Activation-induced changes in platelet surface receptor expression and the contribution of the large-platelet subpopulation to activation.Research and practice in thrombosis and haemostasis · 2020Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The platelet reactivities of two simple collagen-like synthetic peptides, Gly-Lys-Hyp-(Gly-Pro-Hyp)10-Gly-Lys-Hyp-Gly and Gly-Cys-Hyp-(Gly-Pro-Hyp)10-Gly-Cys-Hyp-Gly, were investigated. Both peptides adopted a stable triple-helical conformation in solution. Following cross-linking, both peptides proved to be highly platelet-aggregatory, more active than collagen fibres, inducing aggregation at concentrations as low as 20 ng/ml. These peptides formed microaggregates in solution, and cross-linking was thought to stabilize these structures, allowing expression of their platelet reactivity at 37 degrees C. Like collagen fibres, the peptides caused platelet secretion and release of arachidonate from platelet membrane lipids as well as activation of integrin alpha IIb beta 3 culminating in aggregation. Monoclonal antibodies directed against the integrin alpha 2 beta 1 failed to prevent aggregation release of arachidonate or platelet adhesion to the peptides. Our results indicate that collagen can activate platelets by a mechanism that is independent of integrin alpha 2 beta 1 and for which collagen tertiary and quaternary structures are sufficient alone for activity without the involvement of highly specific cell-recognition sequences.
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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.