Suppression of tissue factor expression, cofactor activity, and metastatic potential of murine melanoma cells by theN-terminal domain of adenovirus E1A 12S protein

2002 ◽  
Vol 85 (1) ◽  
pp. 54-71 ◽  
Author(s):  
Constanze Voigtländer ◽  
Arlymae Rand ◽  
Su-Ling Liu ◽  
Timothy J. Wilson ◽  
Mark R. Pittelkow ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Metastatic Potential ◽  
Melanoma Cells ◽  
Tissue Factor Expression ◽  
Adenovirus E1a ◽  
Murine Melanoma ◽  
Terminal Domain ◽  
Factor Expression ◽  
Cofactor Activity ◽  
Murine Melanoma Cells

Elucidation of the effect of plumbagin on the metastatic potential of B16F10 murine melanoma cells via MAPK signalling pathway

2020 ◽  
Vol 29 (4) ◽  
pp. 427-435
Author(s):  
Fatima‐Zahra Alem ◽  
Meriem Bejaoui ◽  
Myra O. Villareal ◽  
Boutayna Rhourri‐Frih ◽  
Hiroko Isoda
Keyword(s):  
Metastatic Potential ◽  
Melanoma Cells ◽  
Signalling Pathway ◽  
Mapk Signalling Pathway ◽  
Murine Melanoma ◽  
Mapk Signalling ◽  
Murine Melanoma Cells

The Factor VIII Bypassing Activity of Prothrombin Complex Concentrates: The Roles of Factor VIla and of Endothelial Cell Tissue Factor

1991 ◽  
Vol 66 (05) ◽  
pp. 559-564 ◽  
Author(s):  
Jerome M Teitel
Keyword(s):  
Factor Viii ◽  
Tissue Factor ◽  
Factor Viia ◽  
Factor Xa ◽  
Procoagulant Activity ◽  
Tissue Factor Expression ◽  
Prothrombin Complex Concentrates ◽  
Cell Tissue ◽  
Factor Expression ◽  
Necrosis Factor

SummaryAn experimental model incorporating cultured endothelial cells (EC) was used to study the "factor VIII bypassing" activity of prothrombin complex concentrates (PCC), a property exploited in the treatment of hemophiliacs with alloantibodies to factor VIII. Two PCC preparations were ineffective as stimuli of tissue factor expression by EC. However, incubation with a combination of PCC plus endotoxin (lipopolysaccharide, LPS) or tumor necrosis factor (TNF) induced much greater tissue factor expression than was seen in response to either substance alone. PCC expressed an additional direct procoagulant activity at the EC surface, which could not be attributed to either thrombin or factor Xa, and which was diminished by an anti-tissue factor antibody. Therefore factor VIIa, which was detectable in both PCC preparations, likely provided this additional direct procoagulant activity at the EC surface. We also excluded the possibility that coagulation proteases contained in or generated in the presence of PCC are protected from inactivation by AT III. Therefore, PCC can indirectly bypass factor VIII by enhancing induced endothelial tissue factor expression, and also possess direct procoagulant activity, probably mediated by factor VIIa.

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