EC Number   |
General Information |
Reference |
|---|
   3.4.21.21 | malfunction |
eosinophil counts in the bronchoalveolar lavage fluid of wild-type mice increases after ovalbumin challenge, a response that is diminished in comparably challenged low-expressing coagulation factor VII (FVIItTA/tTA) mice. Levels of T helper type 2 cytokines, IL-4, IL-5, and IL-13, and eosinophil-attracting chemokines, eotaxin and RANTES, are also lower in the ovalbumin-challenged low expression factor VIIa mice. Eosinophils purified from low-FVII mice undergo apoptosis at a faster rate compared with wild-type eosinophils, and eosinophil migration in response to eotaxin is reduced in eosinophils obtained from low expressing factor VIIa mice. Airway hyperresponsiveness and mucous layer thickness are reduced in ovalbumin-treated low expressing factor VIIa mice |
707073 |
| 3.4.21.21 | malfunction |
the small nuclear RNA-U1 (U1+ 5a) mediated rescue of FVII mRNA processing impaired by the 9726 + 5G to A mutation results in an appreciable secretion of functional FVII |
707844 |
| 3.4.21.21 | physiological function |
chronic sleep deprivation in a mouse model reduces, in a reversible manner, the FVII expression levels and activity level, thus influencing the TF/FVIIa activation pathway efficiency |
708632 |
| 3.4.21.21 | physiological function |
factor VIIa induces cell survival and gene transcription by transactivation of the insulin-like growth factor 1 receptor. Binding of coagulation factor VIIa to ist receptor tissue factor protects cancer cells from TNF-related apoptosis inducing ligand-induced apoptosis |
732934 |
| 3.4.21.21 | physiological function |
factor VIIa-induced interaction with integrin controls the release of tissue factor on extracellular vesicles from endothelial cells. Intracellular trafficking controlled by factor FVIIa forcing interaction with integrin beta1 regulates tissue factor availability for release on procoagulant extracellular vesicles |
754519 |
| 3.4.21.21 | physiological function |
following injection in mice, both hepatocytes and Kupffer cells appear to be involved in the hepatic clearance and metabolism of both full-length recombinant factor VIIa and recombinant factor VIIa in complex with at least two plasma protease inhibitors |
718422 |
| 3.4.21.21 | physiological function |
FVIIa causes potentiation of cell repulsion by the Eph tyrosine kinase receptor EphB2 ligand ephrin-B1, demonstrating a proteolytical event to control Eph-mediated cell segregation |
732156 |
| 3.4.21.21 | physiological function |
FVIIa in complex with tissue factor initiates the extrinsic coagulation pathway |
717489 |
| 3.4.21.21 | physiological function |
hepatocytes and Kupffer cells and possibly sinusoidal endothelial cells of the rat liver are shown to be physiologically relevant for the clearance of pharmacological doses of recombinant factor FVIIa in rats |
718412 |
| 3.4.21.21 | physiological function |
surface plasmon resonance results show that recombinant factor VII can depress the integration of EGFP-EGF1 (fusion protein epidermal growth factor 1-enhanced green fluorescent protein) with recombinant tissue factor |
709337 |
