ArticleThe Journal of clinical investigation2005
Mice with a severe deficiency in protein C display prothrombotic and proinflammatory phenotypes and compromised maternal reproductive capabilities.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 70 citations in OpenAlex.
- Activated Protein C and the Retina: From Physiology to Therapeutic Potential.International journal of molecular sciences · 2026Review
- Mapping the complexity of ME/CFS: Evidence for abnormal energy metabolism, altered immune profile, and vascular dysfunction.Cell reports. Medicine · 2025Article
- Protein C deficiency with recurrent systemic thrombosis associated with compound heterozygousAmerican heart journal plus : cardiology research and practice · 2025Article
- A Novel Murine Model Enabling rAAV8-PC Gene Therapy for Severe Protein C Deficiency.International journal of molecular sciences · 2024Article
- Dysregulated haemostasis in thrombo-inflammatory disease.Clinical science (London, England : 1979) · 2022Review
- Thrombin spatial distribution determines protein C activation during hemostasis and thrombosis.Blood · 2022Article
- Coagulopathies and inflammatory diseases: '…glimpse of a Snark'.Current opinion in immunology · 2018Review
- Can adjunctive therapies augment the efficacy of endovascular thrombolysis? A potential role for activated protein C.Neuropharmacology · 2018Review
- Candidate SNP markers of reproductive potential are predicted by a significant change in the affinity of TATA-binding protein for human gene promoters.BMC genomics · 2018Article
- Targeting activated protein C to treat hemophilia.Current opinion in hematology · 2017Review
- Thrombin activation of protein C requires prior processing by a liver proprotein convertase.The Journal of biological chemistry · 2017Article
- S2'-subsite variations between human and mouse enzymes (plasmin, factor XIa, kallikrein) elucidate inhibition differences by tissue factor pathway inhibitor -2 domain1-wild-type, Leu17Arg-mutant and aprotinin.Journal of thrombosis and haemostasis : JTH · 2016Article
- Activated protein C promotes neuroprotection: mechanisms and translation to the clinic.Thrombosis research · 2016Review
- Deficiency of superoxide dismutase impairs protein C activation and enhances susceptibility to experimental thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Activated protein C: biased for translation.Blood · 2015Review
- Antibody SPC-54 provides acute in vivo blockage of the murine protein C system.Blood cells, molecules & diseases · 2013Article
- Loss of the cytoskeletal protein Pdlim7 predisposes mice to heart defects and hemostatic dysfunction.PloS one · 2013Article
- Unexpected role of anticoagulant protein C in controlling epithelial barrier integrity and intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Article
- Endogenous protein C is essential for the functional integrity of human endothelial cells.Cellular and molecular life sciences : CMLS · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Anticoagulant protein C (PC) is important not only for maintenance of normal hemostasis, but also for regulating the host immune response during inflammation. Because mice with a designed total genetic deficiency in PC (PC-/- mice) die soon after birth, attempts to dissect PC function in various coagulation/inflammation-based pathologies through use of mice with less than 50% of normal PC levels have not been successful to date. In the current investigation, we have used a novel transgenic strategy to generate different mouse models expressing 1-18% of normal PC levels. In contrast to PC-/- mice, mice with only partial PC deficiency survived beyond birth and also developed thrombosis and inflammation. The onset and severity of these phenotypes vary significantly and are strongly dependent on plasma PC levels. Our findings additionally provide the first evidence that maternal PC is vital for sustaining pregnancy beyond 7.5 days postcoitum, likely by regulating the balance of coagulation and inflammation during trophoblast invasion. These low PC-expressing transgenic mouse lines provide novel animal models that can be used to elucidate the importance of PC in maintenance of the organism and in disease.
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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.