ArticleJournal of thrombosis and haemostasis : JTH2012
A role for adhesion and degranulation-promoting adapter protein in collagen-induced platelet activation mediated via integrin α(2) β(1).
Article in Journal of thrombosis and haemostasis : JTH, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Platelet WDR1 suppresses platelet activity and is associated with cardiovascular disease.Blood · 2016Trial
- Inhibition of LSD1 enhances T cells anti-tumor immunity by promoting TNFSF14 expression in gastric cancer.Molecular and cellular biochemistry · 2026Article
- Platelet Membrane Receptors and Signalling Pathways.Handbook of experimental pharmacology · 2026Review
- FYB1-targeted modulation of CAPG promotes AML progression.Molecular and cellular biochemistry · 2025Article
- ADAP restraint of STAT1 signaling regulates macrophage phagocytosis in immune thrombocytopenia.Cellular & molecular immunology · 2022Article
- Platelet electrical resistance for measuring platelet activation and adhesion in human health and disease.Thrombosis research · 2021Article
- Characterization of Mice with a Platelet-Specific Deletion of the Adapter Molecule ADAP.Molecular and cellular biology · 2019Article
- Immune Cell-Type Specific Ablation of Adapter Protein ADAP Differentially Modulates EAE.Frontiers in immunology · 2019Article
- Functional cyclophilin D moderates platelet adhesion, but enhances the lytic resistance of fibrin.Scientific reports · 2018Article
- Citalopram inhibits platelet function independently of SERT-mediated 5-HT transport.Scientific reports · 2018Article
- Non-small-cell lung cancer cells combat epidermal growth factor receptor tyrosine kinase inhibition through immediate adhesion-related responses.OncoTargets and therapy · 2016Article
- Recessive thrombocytopenia likely due to a homozygous pathogenic variant in the FYB gene: case report.BMC medical genetics · 2014Article
- A role of cell adhesion molecules and gelatinases in human serum-induced aggregation of human eyelid-derived stem cells in vitro.Development & reproduction · 2013Article
- Measurement of the Interaction Between Recombinant I-domain from Integrin alpha 2 beta 1 and a Triple Helical Collagen Peptide with the GFOGER Binding Motif Using Molecular Force Spectroscopy.International journal of molecular sciences · 2013Article
- Crosslinking and composition influence the surface properties, mechanical stiffness and cell reactivity of collagen-based films.Acta biomaterialia · 2012Article
- Mapping of potent and specific binding motifs, GLOGEN and GVOGEA, for integrin α1β1 using collagen toolkits II and III.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundCollagen-induced platelet activation is a key step in the development of arterial thrombosis via its interaction with the receptors glycoprotein (GP)VI and integrin α(2) β(1) . Adhesion and degranulation-promoting adapter protein (ADAP) regulates α(IIb) β(3) in platelets and α(L) β(2) in T cells, and is phosphorylated in GPVI-deficient platelets activated by collagen.
objectivesTo determine whether ADAP plays a role in collagen-induced platelet activation and in the regulation and function of α(2) β(1).
methodsUsing ADAP(-/-) mice and synthetic collagen peptides, we investigated the role of ADAP in platelet aggregation, adhesion, spreading, thromboxane synthesis, and tyrosine phosphorylation. RESULTS AND
conclusionsPlatelet aggregation and phosphorylation of phospholipase Cγ2 induced by collagen were attenuated in ADAP(-/-) platelets. However, aggregation and signaling induced by collagen-related peptide (CRP), a GPVI-selective agonist, were largely unaffected. Platelet adhesion to CRP was also unaffected by ADAP deficiency. Adhesion to the α(2) β(1) -selective ligand GFOGER and to a peptide (III-04), which supports adhesion that is dependent on both GPVI and α(2) β(1), was reduced in ADAP(-/-) platelets. An impedance-based label-free detection technique, which measures adhesion and spreading of platelets, indicated that, in the absence of ADAP, spreading on GFOGER was also reduced. This was confirmed with non-fluorescent differential-interference contrast microscopy, which revealed reduced filpodia formation in ADAP(-/-) platelets adherent to GFOGER. This indicates that ADAP plays a role in mediating platelet activation via the collagen-binding integrin α(2) β(1). In addition, we found that ADAP(-/-) mice, which are mildly thrombocytopenic, have enlarged spleens as compared with wild-type animals. This may reflect increased removal of platelets from the circulation.
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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.