ArticleJournal of thrombosis and haemostasis : JTH2010
Platelet endothelial cell adhesion molecule-1 regulates collagen-stimulated platelet function by modulating the association of phosphatidylinositol 3-kinase with Grb-2-associated binding protein-1 and linker for activation of T cells.
Article in Journal of thrombosis and haemostasis : JTH, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 46 citations in OpenAlex.
- Beyond Hemostasis: Platelets' Multifaceted Functions in Immune Responses.Life (Basel, Switzerland) · 2026Review
- Angiopoietin-like protein 2 inhibits thrombus formation.Molecular and cellular biochemistry · 2025Article
- LAIR-1 and PECAM-1 function via the same signaling pathway to inhibit GPVI-mediated platelet activation.Research and practice in thrombosis and haemostasis · 2024Article
- CD31 as a probable responding and gate-keeping protein of the blood-brain barrier and the risk of Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- CD31 Acts as a Checkpoint Molecule and Is Modulated by FcγR-Mediated Signaling in Monocytes.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Negative regulators of platelet activation and adhesion.Journal of thrombosis and haemostasis : JTH · 2018Review
- Review
- Platelet signaling: a complex interplay between inhibitory and activatory networks.Journal of thrombosis and haemostasis : JTH · 2016Review
- Thymidine phosphorylase participates in platelet signaling and promotes thrombosis.Circulation research · 2014Article
- Identification of functional, short-lived isoform of linker for activation of T cells (LAT).Genes and immunity · 2014Article
- Reactive oxygen species play a critical role in collagen-induced platelet activation via SHP-2 oxidation.Antioxidants & redox signaling · 2014Article
- CD31 is a key coinhibitory receptor in the development of immunogenic dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Article
- Harnessing the platelet signaling network to produce an optimal hemostatic response.Hematology/oncology clinics of North America · 2013Review
- Platelet signaling.Handbook of experimental pharmacology · 2012Review
- An investigation of hierachical protein recruitment to the inhibitory platelet receptor, G6B-b.PloS one · 2012Article
- Regulating thrombus growth and stability to achieve an optimal response to injury.Journal of thrombosis and haemostasis : JTH · 2011Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPlatelet activation by collagen depends on signals transduced by the glycoprotein (GP)VI-Fc receptor (FcR)γ-chain collagen receptor complex, which involves recruitment of phosphatidylinositol 3-kinase (PI3K) to phosphorylated tyrosines in the linker for activation of T cells (LAT). An interaction between the p85 regulatory subunit of PI3K and the scaffolding molecule Grb-2-associated binding protein-1 (Gab1), which is regulated by binding of the Src homology 2 domain-containing protein tyrosine phosphatase-2 (SHP-2) to Gab1, has been shown in other cell types to sustain PI3K activity to elicit cellular responses. Platelet endothelial cell adhesion molecule-1 (PECAM-1) functions as a negative regulator of platelet reactivity and thrombosis, at least in part by inhibiting GPVI-FcRγ-chain signaling via recruitment of SHP-2 to phosphorylated immunoreceptor tyrosine-based inhibitory motifs in PECAM-1.
objectiveTo investigate the possibility that PECAM-1 regulates the formation of the Gab1-p85 signaling complexes, and the potential effect of such interactions on GPVI-mediated platelet activation in platelets.
methodsThe ability of PECAM-1 signaling to modulate the LAT signalosome was investigated with immunoblotting assays on human platelets and knockout mouse platelets.
resultsPECAM-1-associated SHP-2 in collagen-stimulated platelets binds to p85, which results in diminished levels of association with both Gab1 and LAT and reduced collagen-stimulated PI3K signaling. We therefore propose that PECAM-1-mediated inhibition of GPVI-dependent platelet responses result, at least in part, from recruitment of SHP-2-p85 complexes to tyrosine-phosphorylated PECAM-1, which diminishes the association of PI3K with activatory signaling molecules, such as Gab1 and LAT.
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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.