Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Wählen Sie die Spezies und Applikation aus
anti-Mouse (Murine) Factor VII Antikörper:
anti-Human Factor VII Antikörper:
anti-Rat (Rattus) Factor VII Antikörper:
Sie gelangen zu unserer vorgefilterten Suche.
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 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 IHC (p), IHC - ABIN441425
Naderi: Coagulation factor VII is regulated by androgen receptor in breast cancer. in Experimental cell research 2015
Human Monoclonal Factor VII Primary Antibody für ELISA, RIA - ABIN4264232
Mahlangu, Paz, Hardtke, Aswad, Schroeder: TRUST trial: BAY 86-6150 use in haemophilia with inhibitors and assessment for immunogenicity. in Haemophilia : the official journal of the World Federation of Hemophilia 2016
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
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
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
true circadian rhythms for FVII were found
Data suggest that long-term expression of murine activated factor VII (zeige TH Antikörper) is safe, but elevated levels cause premature mortality.
tissue factor (zeige F3 Antikörper)/Factor VIIa/PAR2 (zeige F2RL1 Antikörper) signaling mediates neutrophil activation and fetal death in antiphospholipid syndrome and that statins may be a good treatment for women with aPL (zeige FASL Antikörper)-induced pregnancy complications.
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 (zeige GSK3b Antikörper) 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 (zeige PROC Antikörper)-akt (zeige AKT1 Antikörper); GSK3b (zeige GSK3b Antikörper) = glycogen synthase kinase 3 beta (zeige GSK3b Antikörper))
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 (zeige TH Antikörper) 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 (zeige PROZ Antikörper) rs2273971, and haplotypes GA, CG, and CGA (zeige CGA Antikörper) of Protein Z (zeige PROZ Antikörper) and factor VII (zeige TH Antikörper) had a significant effect on cerebral hemorrhage susceptibility.
Circulating FVII, FVIIa and TFPI (zeige TFPI Antikörper) 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 (zeige F10 Antikörper) 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 (zeige F3 Antikörper) and Factor VIIa.
Data suggest that allosteric regulation of FVIIa activity by tissue factor/thromboplastin (zeige F3 Antikörper) binding appear to involve direct interaction with FVIIa active site, stabilizing segment 215-217, activating loop 3, and leading to enhanced FVIIa activity.
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