ArticleBlood2014
Targeted mutagenesis of zebrafish antithrombin III triggers disseminated intravascular coagulation and thrombosis, revealing insight into function.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 77 citations in OpenAlex.
- The zebrafish model tackles anti-P2Y12 variability in humans: a translational approach.Blood advances · 2026Article
- Impaired cellular trafficking of a thrombomodulin mutant causes severe bleeding, thrombosis, and atypical hemolytic uremic syndrome.Blood vessels, thrombosis & hemostasis · 2026Article
- Dabigatran Prevents Lipopolysaccharide-Mediated Apoptosis in Zebrafish Through a Thrombin-Independent Mechanism.Shock (Augusta, Ga.) · 2026Article
- A sensitized model of thrombosis validates known multigenic relationships and suggests novel modifiers of hemostasis.bioRxiv : the preprint server for biology · 2026Article
- SERPINC1 mutations and thrombotic events in inherited antithrombin deficiency: a study on the han population of East China.Orphanet journal of rare diseases · 2026Article
- β-Antithrombin Levels in Patients with Venous Thromboembolism.International journal of molecular sciences · 2025Article
- FDA-approved drug repurposing in zebrafish identifies thyroid hormone and other compounds as potential antithrombotics.bioRxiv : the preprint server for biology · 2025Article
- Multipopulation GWAS for venous thromboembolism identifies novel loci followed by experimental validation in zebrafish.Blood advances · 2025Article
- Loss of factor VIII in zebrafish rebalances antithrombin deficiency but has a limited bleeding diathesis.Blood advances · 2025Article
- Real-time imaging of blood coagulation and angiogenesis during development in a zebrafish model of type I antithrombin deficiency.Scientific reports · 2025Article
- Loss of protein C vs protein S results in discrepant thrombotic phenotypes.Blood advances · 2025Article
- Hormone-induced thrombosis is mediated through non-canonical fibrin(ogen) aggregation and a novel estrogen target in zebrafish.bioRxiv : the preprint server for biology · 2024Article
- SCAR-6 elncRNA locus epigenetically regulates PROZ and modulates coagulation and vascular function.EMBO reports · 2024Article
- Magnetically powered microwheel thrombolysis of occlusive thrombi in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Loss of factor VIII in zebrafish rebalances antithrombin deficiency but has a limited bleeding diathesis.bioRxiv : the preprint server for biology · 2024Article
- Magnetically Powered Microwheel Thrombolysis of Occlusive Thrombi in Zebrafish.bioRxiv : the preprint server for biology · 2023Article
- Identification and characterization of two SERPINC1 mutations causing congenital antithrombin deficiency.Thrombosis journal · 2023Article
- Computational analyses reveal fundamental properties of the AT structure related to thrombosis.Bioinformatics advances · 2023Article
- Genetic duplication of tissue factor reveals subfunctionalization in venous and arterial hemostasis.PLoS genetics · 2022Article
- Fishing for answers to hemostatic and thrombotic disease: Genome editing in zebrafish.Research and practice in thrombosis and haemostasis · 2022Review
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13 authors at 4 institutions in 1 country.
Funding
Abstract
Pathologic blood clotting is a leading cause of morbidity and mortality in the developed world, underlying deep vein thrombosis, myocardial infarction, and stroke. Genetic predisposition to thrombosis is still poorly understood, and we hypothesize that there are many additional risk alleles and modifying factors remaining to be discovered. Mammalian models have contributed to our understanding of thrombosis, but are low throughput and costly. We have turned to the zebrafish, a tool for high-throughput genetic analysis. Using zinc finger nucleases, we show that disruption of the zebrafish antithrombin III (at3) locus results in spontaneous venous thrombosis in larvae. Although homozygous mutants survive into early adulthood, they eventually succumb to massive intracardiac thrombosis. Characterization of null fish revealed disseminated intravascular coagulation in larvae secondary to unopposed thrombin activity and fibrinogen consumption, which could be rescued by both human and zebrafish at3 complementary DNAs. Mutation of the human AT3-reactive center loop abolished the ability to rescue, but the heparin-binding site was dispensable. These results demonstrate overall conservation of AT3 function in zebrafish, but reveal developmental variances in the ability to tolerate excessive clot formation. The accessibility of early zebrafish development will provide unique methods for dissection of the underlying mechanisms of thrombosis.
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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.