Affinage

F3

Tissue factor · UniProt P13726

Round 2 corrected Audit flag: wrong gene
Length
295 aa
Mass
33.1 kDa
Annotated
2026-04-28
130 papers in source corpus 34 papers cited in narrative 34 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

Tissue factor (TF/F3) is a transmembrane glycoprotein that serves as the primary cellular initiator of blood coagulation by forming a high-affinity 1:1 complex with Factor VIIa, allosterically activating FVIIa to cleave Factors IX and X and triggering a two-phase coagulation cascade of initiation and propagation (PMID:3527261, PMID:8598903, PMID:12070020). TF exists in two functionally distinct cell-surface pools governed by the redox state of its Cys186–Cys209 disulfide bond: a procoagulant pool requiring the intact disulfide and a cryptic/signaling pool in which protein disulfide isomerase disrupts the bond, switching TF to PAR2-dependent signaling that activates G12/G13–Jak2–STAT5–BclXL survival and ERK/CREB pathways (PMID:16959886, PMID:15016732, PMID:18647225). Beyond hemostasis, TF promotes cell adhesion and migration through cytoplasmic-domain phosphorylation-dependent binding to filamin A, drives oncogene (K-ras/p53)-regulated tumor growth and angiogenesis, and mediates immune evasion by inducing platelet aggregation that suppresses NK-cell cytotoxicity (PMID:9490735, PMID:15494427, PMID:35064016). TF-bearing microparticles released from activated platelets, tumor cells, and neutrophil extracellular traps propagate thrombosis in cancer and inflammatory settings including COVID-19, where complement-driven NETosis and P-selectin-mediated platelet–monocyte interactions induce monocyte TF expression (PMID:19861441, PMID:32759504, PMID:32678428).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1986 High

    Establishing how TF engages its enzymatic partner resolved the stoichiometry and lipid dependence of the initiating coagulation complex: FVIIa binds TF at 1:1 stoichiometry in phospholipid vesicles, with phosphatidylserine inducing cooperative binding consistent with at least dimeric TF.

    Evidence Reconstitution of purified TF in phospholipid vesicles with radiolabeled FVII/FVIIa binding and cooperative modeling

    PMID:3527261

    Open questions at the time
    • Whether TF dimers are physiologically relevant on cell membranes was not resolved
    • Allosteric mechanism of FVIIa activation not yet defined
  2. 1987 High

    Molecular cloning revealed TF as a single-pass transmembrane protein of 295 amino acids, providing the sequence foundation for all subsequent structure–function studies.

    Evidence cDNA cloning, Southern/Northern blotting, and sequence analysis

    PMID:3297348

    Open questions at the time
    • Three-dimensional structure unknown
    • Function of the cytoplasmic domain undefined
  3. 1989 High

    Defining where TF is expressed in vivo answered how the body confines coagulation initiation to sites of vascular breach: TF is constitutively present in a hemostatic envelope (adventitia, organ capsules, epidermis) but absent from endothelium, and is inducible in monocytes and enriched in atherosclerotic plaque foam cells.

    Evidence Systematic immunohistochemistry with monoclonal antibodies across normal tissues and atherosclerotic plaques; in situ hybridization

    PMID:2704749 PMID:2719077

    Open questions at the time
    • Mechanism of TF induction in monocytes and plaque cells was uncharacterized
    • Contribution of plaque TF to acute thrombotic events not yet tested in vivo
  4. 1990 High

    Identification of TFPI as a Kunitz-type inhibitor of the TF:FVIIa complex established the primary physiological negative regulator of TF-initiated coagulation.

    Evidence Biochemical inhibition assays with purified TF, FVIIa, and TFPI

    PMID:2271516

    Open questions at the time
    • Relative contributions of TFPI isoforms (α vs β) on different cell surfaces not yet defined
    • In vivo significance not directly tested at this stage
  5. 1995 High

    Demonstrating that NF-κB is obligatory for TF transcriptional induction by LPS, TNF-α, and IL-1β connected TF expression to inflammatory signaling, explaining how inflammation triggers coagulation.

    Evidence PDTC (NF-κB inhibitor) dose-dependently abolished TF mRNA and activity in HUVECs stimulated with multiple agonists

    PMID:7605983

    Open questions at the time
    • Specific NF-κB subunits and promoter elements not mapped in this study
    • Whether NF-κB is the sole transcriptional regulator of TF not addressed
  6. 1996 High

    The 2.0 Å crystal structure of the TF:FVIIa complex revealed how TF allosterically activates FVIIa by stabilizing its extended conformation, answering the central question of how a receptor converts an inert zymogen into an active protease.

    Evidence X-ray crystallography of active-site-inhibited FVIIa bound to soluble TF extracellular domain

    PMID:8598903

    Open questions at the time
    • Structure used truncated soluble TF lacking transmembrane/cytoplasmic domains and membrane context
    • Substrate (FIX/FX) positioning in the complex unknown
  7. 1998 High

    Discovery that TF's cytoplasmic domain binds filamin A (ABP-280) in a phosphorylation-dependent manner and supports cell adhesion/migration established TF as a signaling receptor beyond its coagulation role.

    Evidence Yeast two-hybrid screen, co-immunoprecipitation, Ser→Ala mutagenesis, and functional adhesion/migration assays

    PMID:9490735

    Open questions at the time
    • Kinase(s) responsible for cytoplasmic Ser phosphorylation not identified
    • In vivo relevance of TF–filamin interaction for migration not shown
  8. 2002 High

    Quantitative kinetic analysis of whole-blood TF-initiated coagulation defined two mechanistic phases—initiation (~26 nM thrombin) and propagation—with distinct thrombin thresholds sequentially activating platelets, FXIII, and fibrinogen, providing a quantitative framework for how TF triggers clot formation.

    Evidence Contact-pathway-inhibited whole blood assay measuring TAT, prothrombin fragments, fibrinopeptides, and platelet markers in 20 subjects

    PMID:12070020

    Open questions at the time
    • Contribution of alternatively spliced TF to these phases not examined
    • Role of microparticle TF in propagation phase not addressed
  9. 2003 High

    Identification of alternatively spliced soluble TF (asHTF) in blood and TF on platelet-derived microvesicles revealed that circulating TF pools exist beyond the tissue-fixed hemostatic envelope, fundamentally expanding the concept of TF-mediated thrombosis.

    Evidence RT-PCR identification of splice variant, recombinant protein procoagulant assays, flow cytometry sorting of platelet microvesicles (CD42b+), immunoelectron microscopy of platelet α-granules

    PMID:12514112 PMID:12652293

    Open questions at the time
    • Relative contribution of soluble vs microvesicle TF to in vivo thrombosis not quantified
    • Mechanism by which platelet TF becomes procoagulant upon activation not fully resolved
  10. 2004 High

    Two concurrent discoveries established TF as an effector of oncogenic signaling: K-ras/p53 regulate TF via MEK/PI3K to drive tumor angiogenesis, and TF:FVIIa activates a G12/G13–Jak2–STAT5–BclXL cell survival pathway, revealing non-hemostatic TF functions in cancer.

    Evidence Isogenic K-ras/p53 colorectal lines with TF siRNA and xenograft assays; STAT5 reporters with G-protein and Jak inhibitors and dominant-negatives

    PMID:15016732 PMID:15494427

    Open questions at the time
    • Whether G12/G13–Jak2–STAT5 signaling operates through PAR2 specifically was not fully resolved
    • Relative importance of TF coagulant vs signaling functions in tumor progression in patients unknown
  11. 2006 High

    The discovery that TF's Cys186–Cys209 disulfide bond acts as a redox switch—toggled by PDI in a nitric oxide–dependent manner—between a coagulant and a PAR2-signaling pool resolved how a single receptor can serve dual functions and opened the concept of 'cryptic' TF.

    Evidence Disulfide mutagenesis (C209A), PDI inhibition, NO pathway manipulation, conformation-selective monoclonal antibody blocking coagulation vs signaling readouts

    PMID:16959886

    Open questions at the time
    • Structural basis of conformational change upon disulfide disruption not determined at atomic resolution
    • Proportion of cryptic vs coagulant TF on different cell types in vivo unknown
  12. 2006 High

    Demonstration that platelets constitutively carry TF pre-mRNA and that activation triggers Clk1-dependent splicing to produce functional TF protein revealed a novel post-transcriptional mechanism for rapid TF generation at sites of thrombosis.

    Evidence RT-PCR for pre-mRNA and mature mRNA in resting vs activated platelets, Clk1 pharmacological inhibition, procoagulant/clot assays

    PMID:17060476

    Open questions at the time
    • Physiological contribution of platelet-spliced TF relative to tissue-derived TF in hemostasis not quantified
    • Clk1 substrates in this context not comprehensively mapped
  13. 2007 High

    Showing that TF associates with β1/α3β1 integrins and that a signaling-selective anti-TF antibody suppresses tumor growth as effectively as a coagulation-blocking antibody established that direct TF:FVIIa–PAR2 signaling is required for primary tumor growth independently of downstream coagulation.

    Evidence Co-immunoprecipitation of TF with integrins, isotype-matched signaling- vs coagulation-blocking antibodies, two in vivo xenograft models

    PMID:17901245

    Open questions at the time
    • Structural basis of TF–integrin interaction undefined
    • Whether integrin association modulates the cryptic/coagulant TF switch unknown
  14. 2009 High

    Detection of tumor-derived TF-positive microparticles (co-expressing MUC-1) in cancer patient blood, their elimination by tumor resection, and their association with venous thromboembolism (OR 3.72) provided direct clinical evidence that tumor-shed TF microparticles drive cancer-associated thrombosis.

    Evidence Impedance-based flow cytometry in pancreatic cancer patients, case-control design, tumor resection as intervention

    PMID:19861441

    Open questions at the time
    • Whether TF-positive microparticle levels can serve as a clinically useful biomarker not validated prospectively
    • Functional activity of individual microparticles not measured
  15. 2012 High

    In vivo demonstration that PDI associates with cell-surface TF and that P2X7 receptor-dependent PDI activity is required for TF-dependent arterial thrombosis and procoagulant microparticle biogenesis connected the cryptic TF redox switch to a physiological thrombotic phenotype.

    Evidence Co-IP of PDI with TF, P2X7 knockout mice, FeCl3 carotid thrombosis model, thiol-modifying agents, microparticle activity assays

    PMID:22401798

    Open questions at the time
    • Precise molecular mechanism of P2X7-PDI-TF coupling not defined
    • Whether other thiol oxidoreductases contribute in vivo not excluded
  16. 2018 High

    NETs were established as TF delivery vehicles in thromboinflammation: cathepsin G on NETs cleaves pro-IL-1α to activate endothelial TF expression, and in SLE, REDD1-driven autophagy enhances NET release carrying TF, linking innate immunity, inflammation, and coagulation.

    Evidence NET-endothelial co-culture with cathepsin G and IL-1α blocking; SLE patient neutrophils with autophagy assessment and hydroxychloroquine inhibition

    PMID:29976772 PMID:30563869

    Open questions at the time
    • Relative contribution of NET-borne TF vs monocyte-derived TF in vivo thrombosis not quantified
    • Whether NET-TF pathway is targetable therapeutically in humans not tested
  17. 2020 High

    COVID-19 studies delineated a complement→C5aR1→NETosis→TF pathway and a P-selectin-mediated platelet–monocyte contact mechanism for monocyte TF induction, establishing TF as a central effector of immunothrombosis in SARS-CoV-2 infection.

    Evidence Compstatin C3 inhibition, C5aR1 blockade, NETosis inhibitors in patient neutrophils; flow cytometry with P-selectin and αIIbβ3 blocking in patient monocytes

    PMID:32678428 PMID:32759504

    Open questions at the time
    • Whether anti-TF strategies reduce clinical thrombosis in COVID-19 not tested
    • Generalizability to other viral immunothrombotic conditions unknown
  18. 2022 High

    EBV LMP2A was shown to upregulate TF via PI3K/AKT in nasopharyngeal carcinoma, and TF-induced platelet aggregation suppresses NK-cell cytotoxicity, revealing a viral oncogene–TF axis enabling immune evasion that is reversible by TF inhibition in vivo.

    Evidence LMP2A overexpression, PI3K/AKT inhibition, F3 siRNA, platelet aggregation assays, NK cytotoxicity assays, NPC xenograft model with NK-cell transfer

    PMID:35064016

    Open questions at the time
    • Whether this immune evasion mechanism operates in other EBV-driven malignancies not tested
    • Direct structural basis of TF-mediated platelet aggregation unknown
  19. 2024 Medium

    Placing TF downstream of the Nrf2/GSTP1 axis in ferroptotic hepatocellular injury expanded TF's functional repertoire to include regulation of ferroptosis, a non-apoptotic cell death pathway.

    Evidence GSTP1 overexpression/knockdown, Nrf2 inhibitor, lipid ROS/MDA measurement, TEM for ferroptosis morphology in mouse stress model and AML-12 hepatocytes

    PMID:38890797

    Open questions at the time
    • Mechanism by which TF promotes ferroptosis is not defined at molecular level
    • Single study, not independently replicated
    • Whether TF's role in ferroptosis is coagulation-dependent or signaling-dependent unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the atomic-resolution structure of full-length membrane-bound TF (including the transmembrane and cytoplasmic domains), the identity of kinases that phosphorylate the TF cytoplasmic domain in vivo, the quantitative contribution of each TF pool (tissue-fixed, microparticle, platelet-spliced, alternatively spliced soluble) to hemostasis vs pathological thrombosis, and whether therapeutic targeting of TF signaling can be separated from hemostatic TF function in patients.
  • Full-length TF structure with membrane context unavailable
  • Cytoplasmic domain kinase(s) unidentified
  • Clinical translation of signaling-selective TF inhibition not achieved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 4 GO:0048018 receptor ligand activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005886 plasma membrane 4 GO:0005576 extracellular region 3 GO:0031410 cytoplasmic vesicle 3 GO:0005856 cytoskeleton 1 GO:0031012 extracellular matrix 1
Pathway
R-HSA-109582 Hemostasis 9 R-HSA-162582 Signal Transduction 6 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4
Partners
F2RL1F7FLNAITGB1P4HBTFPI
Complex memberships
TF:FVIIa (extrinsic tenase)

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1987 Molecular cloning of the cDNA for human tissue factor (TF/F3) revealed it encodes a 295-amino acid integral membrane protein with a single transmembrane domain that functions as the high-affinity cellular receptor initiating the coagulation protease cascade. cDNA cloning, Southern blotting, Northern blotting, sequence analysis Cell High 3297348
1986 Factor VII (and VIIa) binds to TF reconstituted in phospholipid vesicles at a 1:1 stoichiometry; phosphatidylserine induces positive cooperativity in binding, consistent with TF functioning as at least a dimer with two interacting enzyme-binding sites. Reconstitution of purified TF into phospholipid vesicles, quantitative binding assays with radiolabeled factors VII/VIIa, protease digestion, cooperative binding modeling Biochemistry High 3527261
1989 TF protein is selectively expressed in a hemostatic 'envelope' pattern in normal human tissues — present in vascular adventitia, organ capsules, epidermis, and mucosal epithelium — but absent from endothelium and circulating blood cells; TF expression is inducible in monocytes by LPS, establishing the cellular basis for coagulation initiation upon vascular injury. Immunohistochemistry with epitope-defined monoclonal antibodies in normal human tissues; LPS stimulation of monocytes The American Journal of Pathology High 2719077
1989 TF mRNA and protein are expressed by macrophage foam cells and mesenchymal intimal cells within atherosclerotic plaques, and TF protein is deposited in the extracellular matrix of necrotic cores, establishing atherosclerotic plaque as a source of thrombogenic TF. In situ hybridization with TF-specific riboprobe and immunohistochemistry in human vessels and atherosclerotic plaques Proceedings of the National Academy of Sciences of the United States of America High 2704749
1990 TF activity is regulated by the Kunitz-type inhibitor TFPI (tissue factor pathway inhibitor), which acts in a multivalent manner to inhibit the TF:FVIIa complex and thereby regulate coagulation. Biochemical inhibition assays with purified components Biochemistry High 2271516
1995 NF-κB activation is an obligatory step in TF induction by diverse agonists (LPS, TNF-α, IL-1β, PMA) in endothelial cells; PDTC, a specific NF-κB pathway inhibitor, dose-dependently abrogates TF mRNA and activity induction, acting at the transcriptional level. PDTC inhibitor treatment of HUVEC, TF activity assay, Northern blot for TF mRNA, dose-response analysis Blood High 7605983
1996 Crystal structure of active-site-inhibited factor VIIa complexed with the soluble extracellular domain of TF at 2.0 Å resolution revealed that FVIIa adopts an extended conformation in the complex, providing the molecular basis for understanding how TF allosterically activates FVIIa and positions it to cleave substrates FIX and FX. X-ray crystallography at 2.0 Å resolution Nature High 8598903
1998 TF supports cell adhesion, migration, spreading, and intracellular signaling independently of RGD-mediated integrin pathways; the TF cytoplasmic domain binds actin-binding protein 280 (ABP-280/filamin A), and this interaction requires extracellular TF ligation and Ser phosphorylation-mimicking mutations; Ala mutations of cytoplasmic Ser residues abolish ABP-280 co-precipitation and severely reduce cell spreading, revealing a cytoskeletal signaling pathway. Yeast two-hybrid screening, co-immunoprecipitation, cell adhesion/migration assays, cytoplasmic domain chimeras, site-directed mutagenesis of Ser residues The Journal of Cell Biology High 9490735
2002 Tissue factor-induced blood coagulation proceeds in two phases: an initiation phase generating ~26 nM thrombin at ~1.3 pM prothrombinase, followed by a propagation phase generating thrombin at ~120 pM prothrombinase; clot formation coincides with transition to the propagation phase, and distinct thrombin concentration thresholds trigger sequential activation of platelets, factor XIII, fibrinogen, and other substrates. Contact pathway-inhibited whole blood coagulation assay, quantitative measurement of TAT complexes, prothrombin fragments, fibrinopeptides, factor Va, platelet activation markers over time in 20 individuals Blood High 12070020
2003 An alternatively spliced form of human TF (asHTF) lacking the transmembrane domain is soluble, circulates in blood, exhibits procoagulant activity when exposed to phospholipids, and is incorporated into thrombi, identifying a circulating thrombogenic TF isoform. Identification of alternatively spliced mRNA, recombinant protein production, procoagulant activity assays with phospholipids, thrombus incorporation studies Nature Medicine High 12652293
2003 Intravascular TF is present mainly on circulating microvesicles in plasma, with platelet-derived microvesicles (identified by CD42b sorting) as a major location; TF is stored in platelet α-granules and the open canalicular system, exposed on the surface after platelet activation; functional TF activity on microvesicles and platelets is enabled when they adhere to neutrophils via P-selectin/PSGL-1 and CD18 interactions, and neutrophil-derived reactive oxygen species further support TF activity. Flow cytometry with cell sorting (CD42b), immunoelectron microscopy, subcellular fractionation, TF activity assays, P-selectin/PSGL-1 blocking antibodies FASEB Journal High 12514112
2004 TF expression in colorectal cancer cells is controlled by K-ras oncogene activation and p53 inactivation via MEK/MAPK and PI3K pathways; RNA interference of TF reduces K-ras-dependent tumorigenic and angiogenic phenotype in vivo, establishing TF as an effector of oncogene-driven tumor progression and angiogenesis. Isogenic colorectal cancer cell lines with defined K-ras/p53 status, MEK/PI3K pharmacological inhibition, TF siRNA knockdown, in vivo xenograft tumor/angiogenesis assays, measurement of cell-associated and microvesicle TF activity Blood High 15494427
2004 TF deficiency causes embryonic lethality in mice, and TF:FVIIa complex signaling through protease-activated receptors (PARs) on vascular cells mediates non-hemostatic functions including inflammation, angiogenesis, metastasis, and cell migration. Review integrating mouse genetic knockout studies and cell signaling experiments Arteriosclerosis, Thrombosis, and Vascular Biology High 15117736
2004 FVIIa/TF interaction induces STAT5 phosphorylation, nuclear translocation, and transactivation; this signaling is dependent on FVIIa proteolytic activity but not on the TF cytoplasmic domain, and requires G12/G13 class G proteins and Jak2 (but not Jak1 or Tyk2); FVIIa/TF promotes cell survival through Jak2/STAT5-dependent BclXL production and Jak2-dependent PKB activation. STAT5 reporter assays, phosphorylation/nuclear translocation experiments, specific G protein and Jak inhibitors, dominant-negative constructs, cell survival assays, BclXL/PKB measurements Circulation Research High 15016732
2006 TF exists in two functionally distinct pools on the cell surface controlled by the redox state of the extracellular Cys186–Cys209 disulfide bond: a coagulant pool requiring this disulfide, and a signaling pool (cryptic/noncoagulant) where protein disulfide isomerase (PDI) disrupts the disulfide in a nitric oxide-dependent pathway, switching TF from coagulation to PAR2-dependent cell signaling; a monoclonal antibody specific for cryptic TF inhibits TF:PAR2 complex formation and TF:VIIa signaling without blocking coagulation. Disulfide bond mutagenesis (C209A and other mutants), PDI inhibition, nitric oxide pathway manipulation, PAR2 signaling assays, specific conformation-selective monoclonal antibody blocking experiments Proceedings of the National Academy of Sciences of the United States of America High 16959886
2006 Human platelets express TF pre-mRNA constitutively; platelet activation triggers Cdc2-like kinase 1 (Clk1)-dependent splicing of TF pre-mRNA into mature mRNA, producing TF protein and procoagulant activity that accelerates clot formation; interruption of Clk1 signaling prevents TF accumulation in activated platelets. RT-PCR for pre-mRNA and mature mRNA in resting vs. activated platelets, Clk1 pharmacological inhibition, TF protein detection, procoagulant/clot formation assays The Journal of Experimental Medicine High 17060476
2007 Direct TF:VIIa signaling (independent of coagulation cascade activation) is required for primary tumor growth; TF associates with β1 integrins in epithelial/endothelial cells (regulated by TF extracellular ligand binding) and constitutively with α3β1 integrin in breast cancer cells; a signaling-inhibitory anti-TF antibody (Mab-10H10) disrupts TF–integrin association and TF:VIIa–PAR2 signaling, suppressing tumor xenograft growth as effectively as the coagulation-inhibitory antibody. Isotype-matched antibody pair (Mab-5G9 vs. Mab-10H10) discriminating coagulation vs. signaling TF; co-immunoprecipitation of TF with β1/α3β1 integrins; PAR2 signaling assays; in vivo human xenograft tumor models (2 models) Blood High 17901245
2008 TF:FVIIa induces phosphorylation and activation of the transcription factor CREB via ERK1/2 and PAR2, independently of the TF cytoplasmic domain; in keratinocytes, this leads to upregulation of pro-apoptotic proteins Bak and Puma and induction of apoptosis in a CREB-dependent manner, whereas FXa (but not thrombin) also induces CREB but without apoptosis, revealing cell-type-specific downstream outcomes. CREB phosphorylation and reporter assays in BHK-TF, HaCaT, and HUVEC cells; ERK and PAR2 inhibition; siRNA/dominant-negative approaches; apoptosis assays; comparison with FXa and thrombin Journal of Thrombosis and Haemostasis High 18647225
2009 Tumor-derived TF-bearing microparticles circulate in blood of cancer patients (detected in ~two-thirds of pancreatic carcinoma patients), co-express tumor marker MUC-1, are eliminated by tumor resection, and elevated levels are associated with venous thromboembolism in cancer patients (adjusted OR 3.72), establishing TF-positive microparticles as mediators of cancer-associated thrombosis. Impedance-based flow cytometry for microparticle detection and quantitation in plasma; case-control study; tumor resection experiments; MUC-1 co-staining Clinical Cancer Research High 19861441
2012 TF procoagulant activity is regulated by thiol-disulfide exchange at the cell surface: protein disulfide isomerase (PDI) is associated with cell-surface TF and required for TF-dependent thrombosis in vivo; PDI regulates thiol-dependent biogenesis of procoagulant microparticles released from myeloid cells and smooth muscle cells via the purinergic P2X7 receptor; genetic deletion of P2X7 attenuates FeCl3-induced carotid artery thrombosis in mice. Co-immunoprecipitation of PDI with TF, thiol-modifying agents, P2X7 genetic knockout mice, FeCl3 carotid artery thrombosis model, microparticle procoagulant activity assays Thrombosis Research High 22401798
2013 TFPIα and TFPIβ are both expressed at the surface of breast cancer cells in GPI-anchored form; PI-PLC cleavage of GPI-anchored TFPI releases both isoforms and increases TF activity on the cell surface, demonstrating that GPI-anchored TFPI inhibits TF:FVIIa activity locally; heparin releases TFPIα but not TFPIβ, revealing distinct surface pools. qRT-PCR, ELISA, flow cytometry, immunofluorescence, Western blotting, PI-PLC and heparin treatment, Factor Xa activity assay Journal of Hematology & Oncology High 23320987
2013 Tumor-derived TF-positive microparticles in blood bind to sites of vascular injury and enhance thrombosis in animal models; elevated circulating TF-positive microparticles correlate with venous thrombosis in multiple cancer types, proposing a mechanism for cancer-associated coagulopathy. Review synthesizing animal model studies (MP binding to injury sites, thrombosis enhancement) and clinical correlation data Blood Medium 23798713
2016 Monomeric CRP (mCRP), formed on microvascular endothelial cell membranes from circulating native pentameric CRP in a receptor-dependent and time-dependent fashion, triggers F3 (TF) gene transcription and TF protein expression in microvascular endothelial cells; F3-silenced endothelial cells are unable to form angiotubes; mCRP-induced TF signaling activates AKT and the transcription factor ETS1, leading to CCL2 release and angiogenesis. Confocal microscopy and Western blot for CRP conversion; F3 gene reporter assays; siRNA silencing of F3; angiogenesis tube formation assay; AKT/ETS1 phosphorylation; CCL2 ELISA; in vivo collagen plug angiogenesis model Thrombosis and Haemostasis High 27808345
2017 Computational molecular dynamics simulation of the full-length TF1-263:FVIIa membrane-bound complex revealed novel non-covalent interactions between TF's EGF2 domain and FVIIa not present in the truncated soluble TF crystal structure; TF allosterically modifies each domain of FVIIa through inter- and intra-domain communication, governing catalytic triad orientation and providing additional stability to the FVIIa protease domain. Computational homology modeling and molecular dynamics simulations of full-length TF:FVIIa membrane complex Journal of Biomolecular Structure and Dynamics Low 28150568
2018 NETs decorated with TF and IL-17A promote thrombin generation and fibrosis in SLE; REDD1-driven autophagy in SLE neutrophils leads to enhanced NET release carrying TF; TF-bearing NETs promote coagulation (thromboinflammation) and activate fibroblasts; hydroxychloroquine inhibits NETosis and the associated TF-bearing NET release. Immunofluorescence, immunoblotting, qPCR, ELISA for NET proteins and TF; autophagy assessment; in vitro primary fibroblast culture with NET stimulation; patient biopsy specimens; bosentan/L-ascorbic acid inhibitors; hydroxychloroquine inhibition Annals of the Rheumatic Diseases Medium 30563869
2018 NETs promote endothelial cell (EC) activation and TF expression through IL-1α and cathepsin G: cathepsin G (a serine protease abundant in NETs) cleaves pro-IL-1α to release mature IL-1α, which then upregulates TF mRNA and activity in ECs; anti-TF antibody blocks NET-induced acceleration of plasma clotting. NET-EC co-incubation assays, anti-IL-1α/IL-1Ra/anti-IL-1β antibody blocking, cathepsin G inhibition, TF mRNA/activity measurement, plasma clotting assays under flow Arteriosclerosis, Thrombosis, and Vascular Biology High 29976772
2019 TF promotes hepatocellular carcinoma (HCC) growth in vitro and in vivo by activating both ERK and AKT signaling pathways; TF induces EGFR upregulation, and EGFR inhibition suppresses TF-mediated HCC growth, placing TF upstream of an EGFR/ERK/AKT axis in HCC. In vitro proliferation/growth assays, in vivo xenograft models, ERK/AKT pathway inhibition, EGFR siRNA knockdown and pharmacological inhibition, TF siRNA knockdown, Western blotting Frontiers in Oncology Medium 30931258
2019 Human primary adipocytes express both TF and FVII; the TF/FVIIa complex formed on the adipocyte surface generates active FXa from substrate Factor X, establishing adipocytes as a procoagulant cell type via autocrine TF/FVIIa activity; active site-inhibited FVIIa blocks FXa formation, confirming specificity. Collagenase isolation of primary human adipocytes, 3T3-L1 differentiation, RT-PCR, Western blot, colorimetric FX activation assay, active site-inhibited FVIIa blocking Upsala Journal of Medical Sciences Medium 31407948
2019 Chemotherapy (oxaliplatin) increases TF expression and MMP-9/2 activity in sciatic nerve and blood; L-OHP elevates HSP70 release from macrophages, activating p-p38 and HIF-1α; hirudin (anticoagulant) suppresses TF, p38, HIF-1α, and MMP-9/2, and attenuates chemotherapy-induced peripheral neuropathy (CIPN), implicating an HSP70-TLR4-p38-TF-HIF-1α axis in CIPN pathology. CIPN mouse model, Von Frey testing, gelatin zymography, Western blotting in sciatic nerve and macrophage cell line, hirudin treatment BioMed Research International Low 31380428
2020 Complement C3 inhibition (with compstatin Cp40) disrupts TF expression in neutrophils; COVID-19 neutrophils release NETs carrying active TF; treatment of control neutrophils with COVID-19 platelet-rich plasma generates TF-bearing NETs that induce thrombotic activity in endothelial cells; C5aR1 blockade and NETosis/thrombin inhibition attenuate platelet-mediated NET-driven TF thrombogenicity, establishing a complement→C5aR1→NETosis→TF pathway in COVID-19 immunothrombosis. Plasma TF activity and sC5b-9 measurement, neutrophil TF expression, C5aR1 blockade, compstatin C3 inhibition, NET/HAEC co-culture thrombosis assay, NETosis/thrombin inhibitors The Journal of Clinical Investigation High 32759504
2020 In severe COVID-19, platelet activation and platelet-monocyte aggregate formation drive monocyte TF expression; platelet P-selectin neutralization or αIIb/β3 integrin blockade with abciximab inhibits platelet-dependent monocyte TF induction ex vivo, identifying P-selectin-mediated platelet-monocyte contact as the mechanism for coagulation activation in severe COVID-19. Flow cytometry for platelet activation markers and monocyte TF expression; ex vivo platelet-monocyte co-culture with P-selectin antibody and abciximab inhibition; plasma from COVID-19 patients applied to control platelets Blood High 32678428
2022 EBV infection upregulates F3 (TF) expression in nasopharyngeal carcinoma and EBV-associated gastric carcinoma cells via the EBV latent membrane protein 2A (LMP2A)-PI3K/AKT signaling pathway; F3-mediated platelet aggregation inhibits NK-cell cytotoxic function; F3 inhibition in vivo restores NK-cell antitumor activity and shows therapeutic efficacy in NPC xenograft models. F3 expression analysis by EBV infection and LMP2A overexpression; PI3K/AKT inhibitor experiments; in vitro and in vivo platelet aggregation assays; NK-cell cytotoxicity assays; F3 siRNA knockdown; NPC xenograft mouse model with NK-cell transfer Cancer Research High 35064016
2022 Paeoniflorin activates the Gas6/Axl/SOCS3 axis to upregulate SOCS3, which subsequently inhibits apoptosis signal-regulating kinase 1 (ASK1) phosphorylation and suppresses TF expression in macrophages and endothelial cells, preventing thrombosis and improving radiation enteritis in mice. Laser Doppler flowmetry, RAW264.7 and HUVEC cell experiments, Gas6/Axl/SOCS3 pathway analysis by Western blot, ASK1/TF expression by qPCR and Western blot, siRNA knockdown, in vivo radiation enteritis mouse model Frontiers in Pharmacology Medium 35359871
2024 GSTP1 methylation-mediated silencing promotes stress-induced hepatocellular injury via ferroptosis through a TF/Nrf2 pathway; GSTP1 overexpression reduces TF expression and GPX4 downregulation, whereas GSTP1 knockdown increases TF and promotes ferroptosis; Nrf2 inhibition exacerbates TF-driven ferroptosis, placing TF downstream of the Nrf2/GSTP1 axis in ferroptotic cell death. Mouse restraint stress model, dexamethasone-treated AML-12 hepatocyte model, GSTP1 overexpression and siRNA, Nrf2 inhibitor, DNA methylation sequencing, Western blotting, lipid ROS/MDA measurement, transmission electron microscopy Journal of Cellular and Molecular Medicine Medium 38890797

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1989 Selective cellular expression of tissue factor in human tissues. Implications for disorders of hemostasis and thrombosis. The American journal of pathology 1130 2719077
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
1989 Localization of tissue factor in the normal vessel wall and in the atherosclerotic plaque. Proceedings of the National Academy of Sciences of the United States of America 1094 2704749
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
1996 The crystal structure of the complex of blood coagulation factor VIIa with soluble tissue factor. Nature 670 8598903
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2020 Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis. The Journal of clinical investigation 628 32759504
2020 Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19. Blood 604 32678428
2004 Role of tissue factor in hemostasis, thrombosis, and vascular development. Arteriosclerosis, thrombosis, and vascular biology 505 15117736
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2021 AaMYB15, an R2R3-MYB TF in Artemisia annua, acts as a negative regulator of artemisinin biosynthesis. Plant science : an international journal of experimental plant biology 33 34034870
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