ArticleBlood2012
JAM-A protects from thrombosis by suppressing integrin αIIbβ3-dependent outside-in signaling in platelets.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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.
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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
44 citing papers in PubMed, 82 citations in OpenAlex.
- Homophilic Interactions of Platelet F11R/JAM-A with its Surface-Bound Counterpart Facilitate Thrombus Formation.Thrombosis and haemostasis · 2026Article
- JAM-A: Adhesion Receptor and Signaling Regulator in Atherosclerosis.Current atherosclerosis reports · 2025Review
- ZO-2 seals the deal for platelet tight junctions.Research and practice in thrombosis and haemostasis · 2025Article
- Formation of tight junction-like structures of zonula occludens 2 in platelet-platelet interaction.Research and practice in thrombosis and haemostasis · 2025Article
- The mechanism of oleic acid inhibiting platelet activation stimulated by collagen.Cell communication and signaling : CCS · 2023Article
- The sinusoidal hematopoietic niche is formed by Jam1a via Notch signaling in the zebrafish kidney.iScience · 2023Article
- Structure, signal transduction, activation, and inhibition of integrin αIIbβ3.Thrombosis journal · 2023Review
- Apolipoprotein A-I, elevated in trauma patients, inhibits platelet activation and decreases clot strength.Platelets · 2022Article
- Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease.JACC. Basic to translational science · 2022Article
- The F11 Receptor (F11R)/Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A) in cancer progression.Molecular and cellular biochemistry · 2022Review
- Junctional adhesion molecule-A is dispensable for myeloid cell recruitment and diversification in the tumor microenvironment.Frontiers in immunology · 2022Article
- Junctional Adhesion Molecules: Potential Proteins in Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Where the Action Is-Leukocyte Recruitment in Atherosclerosis.Frontiers in cardiovascular medicine · 2021Review
- Tetraspanins: integrating cell surface receptors to functional microdomains in homeostasis and disease.Medical microbiology and immunology · 2020Review
- Mouse laser injury models: variations on a theme.Platelets · 2020Review
- Targeting Opposing Immunological Roles of the Junctional Adhesion Molecule-A in Autoimmunity and Cancer.Frontiers in immunology · 2020Review
- Impaired Glycoprotein VI-Mediated Signaling and Platelet Functional Responses in CD45 Knockout Mice.Thrombosis and haemostasis · 2019Article
- Platelet integrin αIIbβ3: signal transduction, regulation, and its therapeutic targeting.Journal of hematology & oncology · 2019Review
- Signaling Pathways of Receptors Involved in Platelet Activation and Shedding of These Receptors in Stored Platelets.Advanced pharmaceutical bulletin · 2019Review
- Platelet-Derived Microparticles From Obese Individuals: Characterization of Number, Size, Proteomics, and Crosstalk With Cancer and Endothelial Cells.Frontiers in pharmacology · 2019Article
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4 authors at 2 institutions in 1 country.
Funding
Abstract
Mounting evidence suggests that agonist-initiated signaling in platelets is closely regulated to avoid excessive responses to injury. A variety of physiologic agonists induce a cascade of signaling events termed as inside-out signaling that culminate in exposure of high-affinity binding sites on integrin α(IIb)β(3). Once platelet activation has occurred, integrin α(IIb)β(3) stabilizes thrombus formation by providing agonist-independent "outside-in" signals mediated in part by contractile signaling. Junctional adhesion molecule A (JAM-A), a member of the cortical thymocyte marker of the Xenopus (CTX) family, was initially identified as a receptor for a platelet stimulatory mAb. Here we show that JAM-A in resting platelets functions as an endogenous inhibitor of platelet function. Genetic ablation of Jam-A in mice enhances thrombotic function of platelets in vivo. The absence of Jam-A results in increase in platelet aggregation ex vivo. This gain of function is not because of enhanced inside-out signaling because granular secretion, Thromboxane A2 (TxA2) generation, as well as fibrinogen receptor activation, are normal in the absence of Jam-A. Interestingly, integrin outside-in signaling such as platelet spreading and clot retraction is augmented in Jam-A-deficient platelets. We conclude that JAM-A normally limits platelet accumulation by inhibiting integrin outside-in signaling thus preventing premature platelet activation.
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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.