ArticleThe Journal of experimental medicine2007
Loss of talin1 in platelets abrogates integrin activation, platelet aggregation, and thrombus formation in vitro and in vivo.
Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.
What it found
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Who cites it
144 citing papers in PubMed, 268 citations in OpenAlex.
- A versatile AuNPs@UiO-66-based electrochemiluminescent immunosensing platform for sensitive detection of talin proteins.Mikrochimica acta · 2026Article
- RAP1-RHO small GTPase cross-talk mediates integrindependent and -independent platelet procoagulant response.Haematologica · 2026Article
- Review
- Platelet-derived integrin- and tetraspanin-enriched tethers exacerbate severe inflammation.Science (New York, N.Y.) · 2026Article
- A Novel KGD-Based αIIbβ3 Antagonist Prevents Arterial Thrombosis While Preserving Hemostasis and Avoiding Thrombocytopenia.International journal of molecular sciences · 2025Article
- Talin, a Rap1 effector for integrin activation at the plasma membrane, also promotes Rap1 activity by disrupting sequestration of Rap1 by SHANK3.Journal of cell science · 2025Article
- Biochemical and structural bases for talin ABSs-F-actin interactions.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Advancing Platelet Research Through Live-Cell Imaging: Challenges, Techniques, and Insights.Sensors (Basel, Switzerland) · 2025Review
- Article
- TLN1: an oncogene associated with tumorigenesis and progression.Discover oncology · 2024Review
- How Protein Depletion Balances Thrombosis and Bleeding Risk in the Context of Platelet's Activatory and Negative Signaling.International journal of molecular sciences · 2024Review
- Development of the Integrated Computer Simulation Model of the Intracellular, Transmembrane, and Extracellular Domain of Platelet Integrin αTH open : companion journal to thrombosis and haemostasis · 2024Article
- Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024Review
- Talin-1 inhibits Smurf1-mediated Stat3 degradation to modulate β-cell proliferation and mass in mice.Cell death & disease · 2023Article
- [Molecular dynamics simulation of force-regulated interaction between talin and Rap1b].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023Article
- Article
- The relative importance of platelet integrins in hemostasis, thrombosis and beyond.Haematologica · 2023Review
- ConFERMing the role of talin in integrin activation and mechanosignaling.Journal of cell science · 2023Article
- Review
- The critical role of Rap1-GAPs Rasa3 and Sipa1 in T cells for pulmonary transit and egress from the lymph nodes.Frontiers in immunology · 2023Article
84 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Platelet adhesion and aggregation at sites of vascular injury are essential for normal hemostasis but may also lead to pathological thrombus formation, causing diseases such as myocardial infarction or stroke. Heterodimeric receptors of the integrin family play a central role in the adhesion and aggregation of platelets. In resting platelets, integrins exhibit a low affinity state for their ligands, and they shift to a high affinity state at sites of vascular injury. It has been proposed that direct binding of the cytoskeletal protein talin1 to the cytoplasmic domain of the integrin beta subunits is necessary and sufficient to trigger the activation of integrins to this high affinity state, but direct in vivo evidence in support of this hypothesis is still lacking. Here, we show that platelets from mice lacking talin1 are unable to activate integrins in response to all known major platelet agonists while other cellular functions are still preserved. As a consequence, mice with talin-deficient platelets display a severe hemostatic defect and are completely resistant to arterial thrombosis. Collectively, these experiments demonstrate that talin is required for inside-out activation of platelet integrins in hemostasis and thrombosis.
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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.