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anti-Human Factor VII Antikörper:
anti-Mouse (Murine) Factor VII Antikörper:
anti-Rat (Rattus) Factor VII Antikörper:
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Human Monoclonal Factor VII Primary Antibody für EIA, WB - ABIN951602
Kazama, Pastuszyn, Wildgoose, Hamamoto, Kisiel: Isolation and characterization of proteolytic fragments of human factor VIIa which inhibit the tissue factor-enhanced amidolytic activity of factor VIIa. in The Journal of biological chemistry 1993
Show all 4 Pubmed References
Human Polyclonal Factor VII Primary Antibody für IF (p), IHC (p) - ABIN1385638
Liu, Xue, Tang, Hou, Qi, Chen, Chen, Zhang, Chen, Xu: A simple method for isolating and culturing the rat brain microvascular endothelial cells. in Microvascular research 2013
Human Polyclonal Factor VII Primary Antibody für IHC (p), IHC - ABIN441425
Naderi: Coagulation factor VII is regulated by androgen receptor in breast cancer. in Experimental cell research 2015
Hepsin (zeige HPN Antikörper) plays a physiologically important role in factor VII (zeige TH Antikörper) 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
The current meta-analysis suggested that polymorphism of R353Q in factor VII (zeige TH Antikörper) was not associated with the MI risk.
FVIIa-antithrombin (zeige SERPINC1 Antikörper) levels in early and late preeclampsia
Using protein C-factor VII (zeige TH Antikörper) chimera demonstrate that APC (zeige APC Antikörper) light chain amino acid residues outside the EPCR (zeige PROCR Antikörper)-binding site enable cytoprotective PAR1 (zeige MARK2 Antikörper) signaling.
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 (zeige TH Antikörper) deficiencies.
Polymorphism rs6046 of the FVII gene is associated with the development of fetal growth retardation in Central Russia.
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.
FVIIa-antithrombin (zeige SERPINC1 Antikörper) but not FVIIa is a ligand for LRP1 (zeige LRP1 Antikörper), and LRP1 (zeige LRP1 Antikörper) contributes to the clearance of FVIIa-antithrombin (zeige SERPINC1 Antikörper) in vivo
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 (zeige F10 Antikörper) complex activates FVIII (zeige F8 Antikörper) apart from thrombin (zeige F2 Antikörper) feedback.
Data suggest activation of PAR2 (zeige F2RL1 Antikörper) via FVIIA/TF signaling activates PI3K (zeige PIK3CA Antikörper)/AKT (zeige AKT1 Antikörper) signaling, inactivates GSK3b signaling, leads to accumulation of beta-catenin (zeige CTNNB1 Antikörper), and promotes tumor cell migration/invasion. (PAR2 (zeige F2RL1 Antikörper) = protease-activated receptor 2 (zeige F2RL1 Antikörper); FVIIA = coagulation factor VIIa; TF = tissue factor/thromboplastin (zeige F3 Antikörper); PI3K (zeige PIK3CA Antikörper) = phosphatidylinositol 3-kinase; AKT (zeige AKT1 Antikörper) = proto-oncogene (zeige RAB1A Antikörper) protein c-akt (zeige AKT1 Antikörper); GSK3b = glycogen synthase kinase 3 beta)
Leu8 (zeige SELL Antikörper) is crucial for FVIIa-EPCR (zeige PROCR Antikörper) binding; this study characterizes its interaction in vivo in mice
FVIIa binding to EPCR (zeige PROCR Antikörper) leads to a barrier protective effect in vivo
FVIIa binding to EPCR (zeige PROCR Antikörper) on the endothelium facilitates the transport of FVIIa from circulation to extravascular tissues where TF resides
RNA interference of Serpinc1 (zeige SERPINC1 Antikörper) and/or Proc allows for evaluation of the function of these genes in vivo and provides a novel, controlled mouse model for spontaneous venous thrombosis.
Murine FVIIa binds poorly to murine EPCR (zeige PROCR Antikörper).
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 (zeige EGR1 Antikörper) in FVIIa-mediated regulation of keratinocyte function was confirmed by use of Egr-1 (zeige EGR1 Antikörper)-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 (zeige F3 Antikörper) and is retained for extended time periods.
Gene targeting of tissue factor (zeige F3 Antikörper), factor X, and factor VII (zeige TH Antikörper) in mice: their involvement in embryonic development
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
, serum prothrombin conversion accelerator
, clotting factor
, FVII coagulation protein
, eptacog alfa
, anti-thrombin 3
, serine (or cysteine) proteinase inhibitor, clade C (antithrombin), member 1
, serpin C1
, serpin peptidase inhibitor, clade C, member 1