ArticleBlood2007
Tissue factor activation: is disulfide bond switching a regulatory mechanism?
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 98 citations in OpenAlex.
- Nature-Inspired Redox Shuttle with Regenerable Antioxidant for Efficient All-Perovskite Tandem Solar Cells.Nano-micro letters · 2026Article
- Trained immunity causes myeloid cell hypercoagulability.Science advances · 2025Article
- Tissue factor in cancer-associated thromboembolism: possible mechanisms and clinical applications.British journal of cancer · 2022Review
- ERO1-PDI Redox Signaling in Health and Disease.Antioxidants & redox signaling · 2021Review
- Murine tissue factor disulfide mutation causes a bleeding phenotype with sex specific organ pathology and lethality.Haematologica · 2020Article
- Beyond thrombosis: the impact of tissue factor signaling in cancer.Journal of hematology & oncology · 2020Review
- Protein disulfide isomerase in cardiovascular disease.Experimental & molecular medicine · 2020Review
- Sphingomyelin encrypts tissue factor: ATP-induced activation of A-SMase leads to tissue factor decryption and microvesicle shedding.Blood advances · 2017Article
- Probing for thiol isomerase activity in thrombi.Journal of thrombosis and haemostasis : JTH · 2016Article
- The Aryl Hydrocarbon Receptor is a Critical Regulator of Tissue Factor Stability and an Antithrombotic Target in Uremia.Journal of the American Society of Nephrology : JASN · 2016Article
- The Role of Putative Phosphatidylserine-Interactive Residues of Tissue Factor on Its Coagulant Activity at the Cell Surface.PloS one · 2016Article
- The C-terminal CGHC motif of protein disulfide isomerase supports thrombosis.The Journal of clinical investigation · 2015Article
- Structure-Function Relationship of the Interaction between Tissue Factor and Factor VIIa.Seminars in thrombosis and hemostasis · 2015Review
- Therapeutic implications of protein disulfide isomerase inhibition in thrombotic disease.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- Breast cancer phenotypes regulated by tissue factor-factor VII pathway: Possible therapeutic targets.World journal of clinical oncology · 2014Review
- Synergies of phosphatidylserine and protein disulfide isomerase in tissue factor activation.Thrombosis and haemostasis · 2014Review
- Protein disulfide isomerase in thrombosis and vascular inflammation.Journal of thrombosis and haemostasis : JTH · 2013Review
- Analysis of tissue factor expression in various cell model systems: cryptic vs. active.Journal of thrombosis and haemostasis : JTH · 2013Article
- Disulfide reduction abolishes tissue factor cofactor function.Biochimica et biophysica acta · 2013Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
A majority of tissue factor (TF) on cell surfaces exists in a cryptic form (ie, coagulation function inactive) but retains its functionality in cell signaling. Recent studies have suggested that cryptic TF contains unpaired cysteine thiols and that activation involves the formation of the disulfide bond Cys186-Cys 209 and that protein disulfide isomerase (PDI) regulates TF coagulant and signaling activities by targeting this disulfide bond. This study was carried out to investigate the validity of this novel concept. Although treatment of MDA 231 tumor cells, fibroblasts, and stimulated endothelial cells with the oxidizing agent HgCl(2) markedly increased the cell-surface TF coagulant activity, the increase is associated with increased anionic phospholipids at the cell surface. Annexin V, which binds to anionic phospholipids, attenuated the increased TF coagulant activity. It is noteworthy that treatment of cells with reducing agents also increased the cell surface TF activity. No evidence was found for either detectable expression of PDI at the cell surface or association of TF with PDI. Furthermore, reduction of PDI with the gene silencing had no effect on either TF coagulant or cell signaling functions. Overall, the present data undermine the recently proposed hypothesis that PDI-mediated disulfide exchange plays a role in regulating TF procoagulant and cell signaling functions.
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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.