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The unexplored newly formed interactions between EGF2 and TF provides a possible explanation for TF-induced allosteric activation of FVIIa.
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TF-FVIIa/trypsin-mediated PAR2 activation leads to enhanced MMP-2 expression in human breast cancer cells contributing to tumor progression.
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The current meta-analysis suggested that polymorphism of R353Q in factor VII was not associated with the MI risk.
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The obtained results suggest a possible protective role of Gln353 and -122C alleles in Recurrent Miscarriage.
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FVIIa-antithrombin levels in early and late preeclampsia
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Using protein C-factor VII chimera demonstrate that APC light chain amino acid residues outside the EPCR-binding site enable cytoprotective PAR1 signaling.
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model predicts that small vesicles promote activation of FX by the extrinsic tenase (VIIa/TF) significantly better than large vesicles
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Low levels of FVII:C and FVIIa reflected the degree of consumption of the coagulation factor among paediatric sepsis patients with disseminated intravascular coagulation.
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Report a good correlation between the type of F7 mutation and/or polymorphisms and FVII:C levels, without a direct link between FVII:C and bleeding tendency in factor VII deficiencies.
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Polymorphism rs6046 of the FVII gene is associated with the development of fetal growth retardation in Central Russia.
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A common pathogenic mechanism, possibly a defective folding of the mutant proteins, was triggered by the FVII mutations. The misfolded state led to impaired trafficking of these proteins causing Endoplasmic reticulum retention, which would explain the low to very low FVII plasma levels observed in patients carrying these mutations.
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FVIIa-antithrombin but not FVIIa is a ligand for LRP1, and LRP1 contributes to the clearance of FVIIa-antithrombin in vivo
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Data suggest that, for all coagulation proteins tested (prothrombin, factor X, activated factor VII, activated protein C), tighter binding to lipid bilayers (lower Kd) is observed as the proportion of anionic phospholipid increases. These studies were conducted in high-throughput screening using phospholipid bilayers in nanodiscs with multiplexed silicon photonic sensor (micro-ring resonator) array technology.
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A coagulation initiating pathway is revealed in which the TF-FVIIa-nascent FXa complex activates FVIII apart from thrombin feedback.
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Data suggest activation of PAR2 via FVIIA/TF signaling activates PI3K/AKT signaling, inactivates GSK3b signaling, leads to accumulation of beta-catenin, and promotes tumor cell migration/invasion. (PAR2 = protease-activated receptor 2; FVIIA = coagulation factor VIIa; TF = tissue factor/thromboplastin; PI3K = phosphatidylinositol 3-kinase; AKT = proto-oncogene protein c-akt; GSK3b = glycogen synthase kinase 3 beta)
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heterozygotes for FVII deficiency show rare bleeding manifestations which are also present in the unaffected family members with normal FVII levels. This indicates that Factor VII activity levels played no role in the occurrence of the bleeding symptoms. Furthermore, FVII levels of around 0.40 IU/dl are capable of assuring a normal hemostasis.
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plasma FVIIa-AT has a thrombophilic role in total and cardiovascular mortality risk in patients with clinically stable stable coronary artery
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Family-based association study revealed that the G allele of Protein Z rs2273971, and haplotypes GA, CG, and CGA of Protein Z and factor VII had a significant effect on cerebral hemorrhage susceptibility.
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Circulating FVII, FVIIa and TFPI were significantly elevated in women with severe preeclampsia in the absence of comparable changes in plasma TF levels.
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Our study findings suggest a link between FVII and AR in prostate cancer pathogenesis.
