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our present data provide convincing evidence that FVIIa binding to EPCR elicits anti-inflammatory signaling via a PAR1- and beta-arrestin-1 dependent pathway.
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Hemophagocytic lymphohistiocytosis and congenital factor VII deficiency caused by compound heterozygote mutations of Factor 7 were found in a 50-year old Chinese female patient. Her family members carried the same mutations but were asymptomatic. (Case reports)
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This study demonstrates that -402G/A of FVII may be a risk factor for lower extremity deep venous thrombosis patients in a Chinese Han population.
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The heterozygosity for MTHFR (rs1801133, rs1801131) and FVII (rs6046) polymorphisms, that could determine genetic predisposition to thrombosis, is high in Turkish Cypriot population.
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there is a strong association between ApoC-III and FVIIa-AT levels in coronary artery disease
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Coagulation factor VIIa (FVIIa) elicits TF cytoplasmic domain-dependent proangiogenic cell signaling independent of the alternative PAR2 activator matriptase.
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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.
