anti-Prothrombin (F2) Antikörper

Human Coagulation Factor II (thrombin) (F2) Interaktionspartner

1. Prothrombin conversion is accelerated in the antiphospholipid syndrome and insensitive to thrombomodulin.

2. Mutation p.Tyr434His in F2 segregated with thrombosis within the family. Tyr434His in F2 is at the target site of arthropod bleeding toxin.

3. Thrombin generation increases between the up- and downregulation phases of In Vitro Fertilization (IVF). No correlation between thrombin generation and TFPI was shown during IVF.

4. 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.

5. When endothelial cells are incubated with antiphospholipid antibodies thrombin generation is increased.

6. No significant difference in FVL genotype between patients and controls was observed, whereas high frequencies of PRT G20210A, MTHFR C677T and MTHFR A1298C mutations in the Hb S patients

7. This study proved that Berberine (BBR) is a direct thrombin inhibitor that has activity in inhibiting thrombin-induced platelet aggregation. BBR may be a potential candidate for the development of safe and effective thrombin-inhibiting drugs

8. Thrombin generation had a limited impact as biomarker of venous thromboembolism.

9. results explain the reduced pro-coagulant activity of the W215A mutant and demonstrate the allosteric connection between Trp215, the sodium-binding loop, and the active site

10. Polymorphisms of F2, PROC, PROZ, and F13A1 Genes are Associated With Recurrent Spontaneous Abortion in Chinese Han Women.

11. the prothrombotic activity of FII is the result of a polymorphism and of a missense mutation, whereas that of FV derives only from a polymorphism. The observation that a clotting factor defect may be associated with both bleeding or venous thrombosis depending on the site of the mutation has caused an extensive reevaluation of the blood clotting mechanism.

12. Findings provide evidence for a relationship between two genes-three mutations-of the cardiovascular disease (CVD genes panel and recurrent pregnancy loss (RPL). These genotypes include the heterozygous state of the factor II G20210A mutation.

13. digestion of thrombin by P. aeruginosa elastase leads to the release of the C-terminal thrombin-derived peptide FYT21, which inhibits pro-inflammatory responses to several pathogen-associated molecular patterns.

14. Prothrombin gene mutation is rare in Budd-Chiari syndrome patients in India.

15. In HBV-related cirrhosis, the combination of miR-122, AFP and PIVKA-II enables the identification of patients at higher risk of hepatocellular carcinoma development.

16. Data, including data using network analysis, suggest that angiotensinogen (AGT), mitogen-activated protein kinase-14 (MAPK14), and prothrombin (F2) in placental villous tissues are core factors in early embryonic development; these studies involved proteomics and bioinformatics analysis of altered protein expression in placental villous tissue from early recurrent miscarriage patients in comparison to control tissues.

17. Arg596Gln mutation is a risk factor for Chinese patients with venous thromboembolism due to its moderately decreased clotting activity but strong resistance to antithrombin inhibition.

18. 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.

19. we were not able to confirm the association between the polymorphisms of f5, f2, and mthfr and pregnancy loss in Bosnian women

20. Platelets were activated in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) patients, and such activation was at least partially attributed to the thrombin-protease-activated receptors (PARs) pathway.

Mouse (Murine) Coagulation Factor II (thrombin) (F2) Interaktionspartner

1. These results suggested that the thrombinstimulated synthesis of IL6 was limited by HSP90 in osteoblasts, and that the effects of HSP90 were exerted at the point between Rhokinase and p38 MAPK.

2. Platelet derived microparticles formed in sepsis are a potent inducer of thrombin generation via phosphatidylserine exposure, and activation of both the intrinsic and extrinsic pathway of coagulation.

3. These findings imply that a thrombin-pericyte interaction in the brain could be a significant mechanism responsible for blood-brain barrier dysfunction under obesity-associated diabetic conditions and thus could represent a therapeutic target for central nervous system complications of diabetes.

4. mutations were introduced into the endogenous fII gene, resulting in expression of prothrombin carrying 3 amino acid substitutions (R157A, R268A, and K281A) to limit activation events to yield only fIIa(Meizothrombin) Homozygous fII(MZ) mice are viable, express fII levels comparable with fII(Wild type) mice, and have reproductive success.

5. Biglycan plays a protective role during the progression of atherosclerosis in ApoE-deficient mice by inhibiting thrombin generation.

6. allosteric inhibitor SbO4L targets the glycoprotein Ibalpha-binding and heparin-binding site of thrombin

7. thrombin/PAR-1 interaction regulated MCP-1, TF, MCSF and IL-6 production.

8. Observations illustrate the role of thrombin as a pleiotropic atherogenic molecule under conditions of hypercholesterolemia and suggest the utility of its inhibition with locally acting antithrombin nanoparticle therapeutics.

9. Thrombin-PAR1 signaling, via nitric oxide and EPCR, promotes hematopoietic stem cell (HSC) mobilization.

10. Primary tumor growth by colon cancer cells was reduced by reduction of circulating prothrombin. There were lower mitotic indices and invasiveness. This growth relied upon 2 targets of thrombin-mediated proteolysis, protease: PAR-1 and fibrinogen.

11. Thrombin promotes sustained signaling and inflammatory gene expression through the CDC25 and Ras-associating domains of phospholipase C epsilon.

12. thrombin/PAR1 pathway as a novel target for developing therapeutic strategies to restore synaptic function in the acute phase of ischemic stroke.

13. High Factor IIa expression is associated with multiorgan pathologies in sickle cell disease.

14. Blockage of thrombin exosites with compounds specific for exosite I (hirudin and HD1 aptamer) or exosite II (heparin and HD22 aptamer) impaired the COMP-thrombin interaction, indicating a 2-site binding mechanism.

15. Whole blood thrombin generation assay is capable of detecting a prothrombotic phenotype in Bmal1-KO mice.

16. Fyn, but not Lyn, was required for complete Pyk2 phosphorylation by thrombin.

17. Thrombin cleavage of osteopontin disrupts a pro-chemotactic sequence for dendritic cells, which is compensated by the release of its pro-chemotactic C-terminal fragment.

18. The Ras-related protein, Rap1A, mediates thrombin-stimulated, integrin-dependent glioblastoma cell proliferation and tumor growth.

19. Influenza virus H1N1 activates platelets through FcgammaRIIA signaling and thrombin generation.

20. These results indicate that thrombin acts through multiple mechanisms to activate MMPs and PGE2 synthesis in amnion.

Cow (Bovine) Coagulation Factor II (thrombin) (F2) Interaktionspartner

1. the weaker rapid interaction between prothrombin and membranes is the most important in vivo when considering the activation of prothrombin at the cell surface.

2. novel pyranosic sulfated arabinan Ab1 exerts its anticoagulant activity on thrombin by a mechanism different from those found previously for other sulfated polysaccharides and glycosaminoglycans

3. Exogenous delivery of thrombin enhances microvascular collateral development in response to ischemic insult, and accelerates tissue reperfusion.

4. the signaling pathways of MAPK, MSK1, and NF-kappaB play important roles in thrombin-induced iNOS expression in alveolar macrophages

5. High glucose enhances smooth muscle cell responsiveness to thrombin through transcriptional upregulation of PAR-4, mediated via PKC and NFkappaB.

6. Thrombin induces a sustained contraction in the normal pulmonary artery, by activating PAR(1) and thereby increasing the sensitivity of the myofilament to Ca(2+).

7. kinetic and structural analysis of interactions between thrombin and the Factor XIII activation peptide

8. analysis of staphylocoagulase-mediated bovine prothrombin activation

9. crystal structure

10. thrombin and factor Xa diffusion along the heparin molecule explains the effects of extended heparin chain lengths

11. A comparison of recombinant thrombin to bovine thrombin as a hemostatic ancillary in patients undergoing peripheral arterial bypass and arteriovenous graft procedures.

12. Thrombomoduln not only binds to HMGB1 but also aids the proteolytic cleavage of HMGB1 by thrombin.

13. Examination of a dipalmitoylphosphatidylcholine membrane-bound prothrombin 1 fragment reveals another well-defined carboxyglutamic acid (Gla domain)-binding site for phosphatidylserine.

14. These studies illustrate that GpIbalpha and gamma' target thrombin binding sites with similar consequences on thrombin dynamics, albeit with differing structural features.

15. ERK-dependent IKKalpha/beta/NF-kappaB signaling pathway plays an important role in thrombin-induced COX-2 expression in human lung fibroblasts.

Zebrafish Coagulation Factor II (thrombin) (F2) Interaktionspartner

1. Prothrombin morpholino-injected zebrafish embryos yielded an early phenotype exhibiting severe abnormalities that later showed occasional bleeding

Rhesus Monkey Coagulation Factor II (thrombin) (F2) Interaktionspartner

1. The great similarity of prothrombin among rhesus, human, and porcine confirm the great value of the pig-to-rhesus xenotransplantation model.

Pig (Porcine) Coagulation Factor II (thrombin) (F2) Interaktionspartner

1. thrombin stimulates transglutaminase activity in articular cartilage by directly cleaving factor XIII and by receptor-mediated up-regulation of factor XIII synthesis

2. The great similarity of prothrombin among rhesus, human, and porcine confirm the great value of the pig-to-rhesus xenotransplantation model.

3. In conclusion, thrombin activates pro-MMP-2 in the absence of elevated pro-MMP-2 expression and secretion in CSMCs, and thrombin induces CSMC mitogenesis involving its action on MMP-2

4. Thrombin stimulates swine smooth muscle cell differentiation from peripheral blood mononuclear cells via protease-activated receptor-1, RhoA, and myocardin.