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Coagulation factor II is proteolytically cleaved to form thrombin in the first step of the coagulation cascade which ultimately results in the stemming of blood loss.
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Platelets were activated in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) patients, and such activation was at least partially attributed to the thrombin (show F2 Proteins)-protease-activated receptors (PARs (show EPRS Proteins)) pathway.
The meta-analysis enabled us to underline the importance of DCP (show ACE Proteins) in the refinement of the eligibility criteria of hepatocellular cancer (HCC (show FAM126A Proteins))patients for liver transplant (LT). This information, based on Japanese studies performed in the setting of living-donor LT only, needs further validation in the Western world both in the setting of post-mortem and living-donor LT.
HCC (show FAM126A Proteins) [hepatocellular carcinoma] patients who are sero-positive for DCP (show ACE Proteins) [Des (show DES Proteins)-gamma-carboxyprothrombin] and sero-negative for AFP (show AFP Proteins)[Alpha-fetoprotein (show AFP Proteins)] have significantly higher levels of serum ALT[alanine aminotransferase (show ALT Proteins)]; serum ALT levels may be of diagnostic importance in AFP (show AFP Proteins)-negative, HBV-related HCC (show FAM126A Proteins) [hepatitis B virus-related hepatocellular carcinoma] patients.
Evaluation of initial thrombin (show F2 Proteins) generation is useful to distinguish between beneficial coagulation activation and hazardous haemostatic alteration, and to predict multiorgan dysfunction development and poor outcome in septic patients.
Prothrombin (show F2 Proteins) showed statistically significant differences between the groups of septic and non-septic burn patients.
The data indicate that prothrombin (show F2 Proteins) Arg596 missense mutations lead to antithrombin (show SERPINC1 Proteins) (AT) and thrombomodulin (TM (show THBD Proteins)) resistance in the variant thrombins and suggest that prothrombin (show F2 Proteins) Arg596 is important for AT- and TM-mediated anticoagulation.
application of electrical stimulus modifies the molecular interactions within the complex and consequently, electrical field can be used to modulate the association between the thrombin (show F2 Proteins) and its aptamer.
The G20210A prothrombin (show F2 Proteins) mutation carriers after venous thromboembolism have unfavourable fibrin clot (show TXNDC17 Proteins) characteristics, including lower permeability and impaired lysis compared with non-carriers. Rivaroxaban treatment cannot abolish more prothrombotic fibrin clot (show TXNDC17 Proteins) phenotype observed in prothrombin (show F2 Proteins) mutation carriers following VTE.
prothrombin (show F2 Proteins)-20210-mutations are playing a significant role in the pathogenesis of cerebral sinus vein thrombosis, but not in arterial ischemic stroke
Patients with early onset preeclampsia are characterised by an attenuated coagulation response characterised by reduced thrombin (show F2 Proteins) generation stimulated by low-dose TF and elevated plasma TFPI (show TFPI Proteins) activity.
Platelet derived microparticles formed in sepsis are a potent inducer of thrombin (show F2 Proteins) generation via phosphatidylserine exposure, and activation of both the intrinsic and extrinsic pathway of coagulation.
These findings imply that a thrombin (show F2 Proteins)-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.
mutations were introduced into the endogenous fII gene, resulting in expression of prothrombin (show F2 Proteins) 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.
Biglycan (show BGN Proteins) plays a protective role during the progression of atherosclerosis in ApoE (show APOE Proteins)-deficient mice by inhibiting thrombin (show F2 Proteins) generation.
allosteric inhibitor SbO4L targets the glycoprotein Ibalpha (show GP1BA Proteins)-binding and heparin-binding site of thrombin (show F2 Proteins)
thrombin (show F2 Proteins)/PAR-1 (show MARK2 Proteins) interaction regulated MCP-1 (show CPT1B Proteins), TF, MCSF (show CSF1 Proteins) and IL-6 (show IL6 Proteins) production.
Observations illustrate the role of thrombin (show F2 Proteins) as a pleiotropic atherogenic molecule under conditions of hypercholesterolemia and suggest the utility of its inhibition with locally acting antithrombin (show SERPINC1 Proteins) nanoparticle therapeutics.
Thrombin (show F2 Proteins)-PAR1 (show F2R Proteins) signaling, via nitric oxide and EPCR (show PROCR Proteins), promotes hematopoietic stem cell (HSC (show FUT1 Proteins)) mobilization.
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.
Thrombin (show F2 Proteins) promotes sustained signaling and inflammatory gene expression through the CDC25 (show CDC25C Proteins) and Ras-associating domains of phospholipase C epsilon (show PLCE1 Proteins).
Coagulation factor II is proteolytically cleaved to form thrombin in the first step of the coagulation cascade which ultimately results in the stemming of blood loss. F2 also plays a role in maintaining vascular integrity during development and postnatal life. Mutations in F2 leads to various forms of thrombosis and dysprothrombinemia.
prepro-coagulation factor II
, prothrombin B-chain
, serine protease
, coagulation factor 2