ArticleBlood2009
The tyrosine phosphatase CD148 is an essential positive regulator of platelet activation and thrombosis.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 133 citations in OpenAlex.
- Targeting CD148 for Antithrombotic Therapy: Functional and Molecular Evaluation of AKB-9778.Pharmacology research & perspectives · 2026Article
- Quantitative Flow Cytometry-Medical Applications with a Focus on Blood Platelets.International journal of molecular sciences · 2026Review
- Platelet Membrane Receptors and Signalling Pathways.Handbook of experimental pharmacology · 2026Review
- Relieving platelet inhibition using a novel bispecific antibody: a novel approach for circumventing the platelet storage lesion.Journal of thrombosis and haemostasis : JTH · 2026Article
- Dengue infection changes the expressions of CD154 and CD148 in human platelets.Virus research · 2025Article
- How Protein Depletion Balances Thrombosis and Bleeding Risk in the Context of Platelet's Activatory and Negative Signaling.International journal of molecular sciences · 2024Review
- 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
- Review
- Restraining of glycoprotein VI- and integrin α2β1-dependent thrombus formation by platelet PECAM1.Cellular and molecular life sciences : CMLS · 2024Article
- Multicolor flow cytometry in clinical samples for platelet signaling assessment.Research and practice in thrombosis and haemostasis · 2023Article
- Review
- Experimental validation of computerised models of clustering of platelet glycoprotein receptors that signal via tandem SH2 domain proteins.PLoS computational biology · 2022Article
- PlateletCells · 2022Review
- Review
- Whole genome sequence analysis of platelet traits in the NHLBI Trans-Omics for Precision Medicine (TOPMed) initiative.Human molecular genetics · 2022Article
- Hereditable variants of classical protein tyrosine phosphatase genes: Will they prove innocent or guilty?Frontiers in cell and developmental biology · 2022Review
- AVEXIS technology identifies novel platelet-leukocyte binding partners including CD148-CD300a.Blood advances · 2021Article
- Thromboses and Hemostasis Disorders Associated with COVID-19: The Possible Causal Role of Cross-Reactivity and Immunological Imprinting.Global medical genetics · 2021Article
- Characterization of Cellular Heterogeneity and an Immune Subpopulation of Human Megakaryocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Platelet Src family kinases: A tale of reversible phosphorylation.Research and practice in thrombosis and haemostasis · 2021Review
2 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
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Platelets play a fundamental role in hemostasis and thrombosis. They are also involved in pathologic conditions resulting from blocked blood vessels, including myocardial infarction and ischemic stroke. Platelet adhesion, activation, and aggregation at sites of vascular injury are regulated by a diverse repertoire of tyrosine kinase-linked and G protein-coupled receptors. Src family kinases (SFKs) play a central role in initiating and propagating signaling from several platelet surface receptors; however, the underlying mechanism of how SFK activity is regulated in platelets remains unclear. CD148 is the only receptor-like protein tyrosine phosphatase identified in platelets to date. In the present study, we show that mutant mice lacking CD148 exhibited a bleeding tendency and defective arterial thrombosis. Basal SFK activity was found to be markedly reduced in CD148-deficient platelets, resulting in a global hyporesponsiveness to agonists that signal through SFKs, including collagen and fibrinogen. G protein-coupled receptor responses to thrombin and other agonists were also marginally reduced. These results highlight CD148 as a global regulator of platelet activation and a novel antithrombotic drug target.
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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.