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In diabetics, miR-19a and miR-126 cooperate to exhibit anti-thrombotic properties by epigenetic regulation of tissue factor.
High levels of TF were associated with thrombosis related to antiphospholipid syndrome.
Elevated plasma levels of procoagulant factors, such as FVIII or prothrombin, enhanced thrombin generation and reduced the amount of TF required for the initiation of thrombin formation.
TF knockout in MDA-MB-231cells reduced TF/FVIIa signaling and coagulation activity. Silencing of TF in MDA-MB-231cells decreased the release of microvesicles.
Subjects with AG and GG genotype had significantly higher TF levels than AA genotype. GG genotype of 603A>G polymorphism augments the risk of thrombosis by 4.4 fold, thus highlighting the significance of this polymorphism in the development of DVT
Monocyte TF may be a relevant source of TF-mediated thrombogenicity in NSCLC patients and may be associated with prognosis in NSCLC.
plasma activity higher in women with pre-eclampsia than in those with infants small for gestational age or normal pregnancies
The interaction between tissue factor and filamin A is dependent on the differential phosphorylation of Ser253 and Ser258. The interaction with filamin A may translocate cell surface TF to cholesterol-rich lipid rafts, increasing cell surface TF activity as well as TF incorporation and release into microvesicles.
The induction of TG by BXPC3 cells was mainly driven by the TF pathway while TG generation triggered by MCF7 cells was also driven by FXII activation.
Our study identifies a previously undescribed role of miRNA in venous thrombosis by regulating TF expression. Therefore, restoration of miR-145 levels may serve as a promising therapeutic strategy for management of venous thrombosis
TF(+) microvesicless released from orthotopic pancreatic tumors increase venous thrombosis in mice.
HUVEC and adult human dermal blood endothelial cells respond similarly to TNFalpha and IL-1beta in terms of TF expression, and both are suitable models to examine cell surface TF activity and TF-positive microvesicle release in endothelial cells.
Cell lines with intrinsically high TF expression were associated with decreased cancer stem cell activity. Knockdown of TF was associated with increased cancer stem cell activity. Overexpression of TF was associated with decreased cancer stem cell activity. Expression of TF did not affect cellular viability but may increase proliferation.
uPAR and TF could potentially be attractive targets for molecular imaging and therapy in oral squamous cell carcinoma due to high positive expression rates and tumor-specific expression patterns.
The highest tissue factor activity was detected in microparticles from monocytes, lower activity - in microparticles from endothelial cells and THP-1 cells, and no activity - in microparticles from platelets and granulocytes.
These results demonstrate that procoagulant microvesicles shed by head and neck squamous cell carcinoma line (UMSCC81B) induced a procoagulant effect in HUVECs through increased clotting activity and cell membrane surface expression of TF.
Patients with early onset preeclampsia are characterised by an attenuated coagulation response characterised by reduced thrombin generation stimulated by low-dose TF and elevated plasma TFPI activity.
The proinflammatory cytokine IL-33 induces differential tissue factor expression and activity in monocyte subsets, as well as the release of procoagulant microvesicless. In this manner, IL-33 may contribute to the formation of a prothrombotic state characteristic for cardiovascular disease.
Pin1 is a fast-acting enzyme which may be utilised by cells to protect the phosphorylation state of TF in activated cells prolonging TF activity and release, and therefore ensuring adequate haemostasis.
Circulating pentraxin nCRP has little pro-angiogenic effect but when dissociated into mCRP on the surface of endothelial cells it is able to trigger potent proangiogenic effects by inducing F3-gene upregulation and TF signaling.
f3b is required for brain vascular development and for development of part of the somatic vasculature during embryogenesis in the zebrafish
Tissue factor cytoplasmic domain is involved in TF-PAR-2 signalling initiating hepatic fibrosis and is a potential therapeutic target, as its deletion would not impact coagulation.
Myeloid cell derived tissue factor dampens inflammation in acid-induced acute lung injury.
Ticagrelor, but not clopidogrel, reduces arterial thrombosis via endothelial tissue factor suppression. Ticagrelor reduced TNF-alpha-induced TF expression via proteasomal degradation.
Macrophage tissue factor prothrombotic activity is regulated by integrin-alpha4/arf6 trafficking.
Evening primrose oil and forskolin decreased the prothrombotic effect of celecoxib initiated by a LPS challenge in mice, and this effect was, at least partly, mediated by mitigating TF expression and activity.
There was no significant contribution of TF on myeloid cells in multiple models of experimental ALI, leading to the conclusion that TF in myeloid cells is not a major contributor to experimental ALI.
Hepatocyte TF activates coagulation in a mouse model of chronic liver injury
Thrombin-independent contribution of tissue factor to inflammation and cardiac hypertrophy in a mouse model of sickle cell disease.
expression by myeloid cells affects macrophage differentiation, and regulate Mycobacterium tuberculosis growth
TF expressed on tumor microparticles contributes to the increased incidence of cancer-associated venous thrombosis in mice in vivo.
These findings reveal a novel biological function and mechanism of the protein C pathway in which protein S and the aPC-cleaved form of fV are cofactors for anti-inflammatory cell signaling by aPC in the context of endotoxemia and infection
Lung epithelial tissue factor regulates alveolar procoagulant activity and permeability in acute lung injury.
PGE2 increases both TF expression and activity through the regulation of the EP1/SIRT1 pathway.
Fas-initiated, caspase-3-dependent hepatocyte apoptosis increases tissue factor procoagulant activity through a mechanism involving phosphatidylserine externalization.
Heme promotes tissue factor-dependent coagulation activation and induces tissue factor expression on leukocytes in vivo.
TF is essential for the development of pericyte coverage of tumor microvessels and aPL-induced tumor cell expression of chemokine ligand 2, a mediator of pericyte recruitment
Alternatively spliced tissue factor promotes plaque angiogenesis through the activation of hypoxia-inducible factor-1alpha and vascular endothelial growth factor signaling.
Klkb1(-/-) mice have a novel mechanism for thrombosis protection in addition to reduced contact activation. This pathway arises when bradykinin delivery to vasculature is compromised and mediated by increased receptor Mas, prostacyclin, Sirt1, and KLF4
study provides a novel mechanism for the posttranscriptional regulation of TF expression, indicating that this is selectively regulated by PARP-14.
Mice in which TF gene is disrupted in the neuroectodermal lineage exhibit delayed progression of spontaneous brain tumors driven by oncogenic N-ras and SV40 large T antigen (SV40LT) expressed under the control of sleeping beauty transposase.
Tissue factor expression on porcine neonatal islet cell clusters is an important initiator of instant blood-mediated inflammatory reaction in islet xenotransplantation.
Prolonged clopidogrel treatment reduced coronary tissue factor (TF) expression and tended to reduce the blood TF level post-PCI, thus possibly modulating the risk of late thrombosis.
Procoagulant porcine tissue factor is induced in primary pig aortic endothelial cells only by fresh human plasma, and not by heat-inactivated plasma.
myocardial infarction induced proinflammatory gene and protein expression in peripheral blood mononuclear cells of tissue factor cyclo-oxygenase-2, monocyte chemoattractant protein-1 and CRP
Arterial (18)F-fluorodeoxyglucose uptake reflects balloon catheter-induced thrombus formation and tissue factor expression via nuclear factor-kappaB in rabbit atherosclerotic lesions.
Polycations could present a new class of anticoagulants with such unique upstream downregulation of blood coagulation, selectively blocking tissue factor-dependent factor VII activation.
Upregulated TF expression and increased plasma TF level during reperfusion period, reduced plasma TFPI-1 level during reperfusion period.
Prolonged expression of biologically active rabbit TF was shown within jugular vein grafts of hypercholesterolemic rabbits.
lectin-like oxidized LDL receptor Oxidized low-density lipoprotein receptor 1expression appears to be closely associated with tissue factor expression, apoptotic events and morphological vulnerability in atherosclerotic lesions
This gene encodes coagulation factor III which is a cell surface glycoprotein. This factor enables cells to initiate the blood coagulation cascades, and it functions as the high-affinity receptor for the coagulation factor VII. The resulting complex provides a catalytic event that is responsible for initiation of the coagulation protease cascades by specific limited proteolysis. Unlike the other cofactors of these protease cascades, which circulate as nonfunctional precursors, this factor is a potent initiator that is fully functional when expressed on cell surfaces. There are 3 distinct domains of this factor: extracellular, transmembrane, and cytoplasmic. This protein is the only one in the coagulation pathway for which a congenital deficiency has not been described. Alternate splicing results in multiple transcript variants.
, coagulation factor III
, coagulation factor 3
, brain tissue factor
, coagulation factor IIIb
, coagulation factor III (thromboplastin, tissue factor) S homeolog