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Human Factor VII Protein expressed in Human Cells - ABIN2004310
Li, Wang, Long, Su, Bukhory, Dai, Jin, Huang, Jia, Li, Fan, Liu, Wang: Novel antibody against a glutamic acid-rich human fibrinogen-like protein 2-derived peptide near Ser91 inhibits hfgl2 prothrombinase activity. in PLoS ONE 2014
Hepsin (show HPN Proteins) plays a physiologically important role in factor VII (show TH Proteins) activation and hemostasis in zebrafish.
study reports the full-length cDNA sequences of rhesus monkey FVII; deduced protein sequence of FVII indicates the functional domains; comparison of three-dimensional protein structure with human shows high conservation between them
Leu8 (show SELL Proteins) is crucial for FVIIa-EPCR (show PROCR Proteins) binding; this study characterizes its interaction in vivo in mice
FVIIa-antithrombin (show SERPINC1 Proteins) but not FVIIa is a ligand for LRP1 (show LRP1 Proteins), and LRP1 (show LRP1 Proteins) contributes to the clearance of FVIIa-antithrombin (show SERPINC1 Proteins) in vivo
FVIIa binding to EPCR (show PROCR Proteins) leads to a barrier protective effect in vivo
FVIIa binding to EPCR (show PROCR Proteins) on the endothelium facilitates the transport of FVIIa from circulation to extravascular tissues where TF resides
Murine FVIIa binds poorly to murine EPCR (show PROCR Proteins).
Conclude that the fVII-targeted verteporfin photodynamic therapy that we report here is a novel and effective therapeutic with improved selectivity for the treatment of breast cancer.
The participation of Egr-1 (show EGR1 Proteins) in FVIIa-mediated regulation of keratinocyte function was confirmed by use of Egr-1 (show EGR1 Proteins)-deficient mice, wherein a significant delay in skin wound healing after injury was observed, relative to WT mice.
Recombinant FVIIa readily associates with the vascular endothelium and subsequently enters into extravascular spaces where it is likely to bind to tissue factor (show F3 Proteins) and is retained for extended time periods.
Gene targeting of tissue factor (show F3 Proteins), factor X, and factor VII (show TH Proteins) in mice: their involvement in embryonic development
true circadian rhythms for FVII were found
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.
A coagulation initiating pathway is revealed in which the TF-FVIIa-nascent FXa (show F10 Proteins) complex activates FVIII (show F8 Proteins) apart from thrombin (show F2 Proteins) feedback.
Data suggest activation of PAR2 (show F2RL1 Proteins) via FVIIA/TF signaling activates PI3K (show PIK3CA Proteins)/AKT (show AKT1 Proteins) signaling, inactivates GSK3b signaling, leads to accumulation of beta-catenin (show CTNNB1 Proteins), and promotes tumor cell migration/invasion. (PAR2 (show F2RL1 Proteins) = protease-activated receptor 2 (show F2RL1 Proteins); FVIIA = coagulation factor VIIa; TF = tissue factor/thromboplastin (show F3 Proteins); PI3K (show PIK3CA Proteins) = phosphatidylinositol 3-kinase; AKT (show AKT1 Proteins) = proto-oncogene (show RAB1A Proteins) protein c-akt (show AKT1 Proteins); GSK3b = glycogen synthase kinase 3 beta)
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 (show TH Proteins) 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.
Family-based association study revealed that the G allele of Protein Z (show PROZ Proteins) rs2273971, and haplotypes GA, CG, and CGA (show CGA Proteins) of Protein Z (show PROZ Proteins) and factor VII (show TH Proteins) had a significant effect on cerebral hemorrhage susceptibility.
Circulating FVII, FVIIa and TFPI (show TFPI Proteins) were significantly elevated in women with severe preeclampsia in the absence of comparable changes in plasma TF levels.
Our study findings suggest a link between FVII and AR in prostate cancer pathogenesis.
Large deletions play a minor but essential role in the mutational spectrum of the F7 and F10 (show F10 Proteins) genes. Copy number analyses (e. g. MLPA) should be considered if sequencing cannot clarify the underlying reason of an observed coagulopathy. Of note, in cases of combined FVII/FX deficiency, a deletion of the two contiguous genes might be part of a larger chromosomal rearrangement.
Structure-Function Relationship of the Interaction between Tissue Factor (show F3 Proteins) and Factor VIIa.
This gene encodes coagulation factor VII which is a vitamin K-dependent factor essential for hemostasis. This factor circulates in the blood in a zymogen form, and is converted to an active form by either factor IXa, factor Xa, factor XIIa, or thrombin by minor proteolysis. Upon activation of the factor VII, a heavy chain containing a catalytic domain and a light chain containing 2 EGF-like domains are generated, and two chains are held together by a disulfide bond. In the presence of factor III and calcium ions, the activated factor then further activates the coagulation cascade by converting factor IX to factor IXa and/or factor X to factor Xa. Defects in this gene can cause coagulopathy. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
coagulation factor VII
, clotting factor
, serum prothrombin conversion accelerator
, FVII coagulation protein
, eptacog alfa