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- W2018360947 abstract "Antithrombin (AT) is the physiological inhibitor of thrombin or other serine proteases of coagulation cascades. AT is also known to regulate inflammatory reactions. To determine whether AT inhibits cytokine-induced endothelial activation, we examined the effect of AT on an increase in endothelial cell adhesion molecules E-selectin and intercellular adhesion molecule-1 induced by tumor necrosis factor (TNF)-α. AT inhibited increase in E-selectin and intercellular adhesion molecule-1 expression induced by tumor necrosis factor-α. AT inhibited neither IκB degradation, nuclear translocation of NF-κB, nor nuclear binding activity of NF-κB. This suggests that AT did not inhibit the NF-κB pathway. AT inhibited physical interaction of p65 with p300, nuclear cofactor of NF-κB. Intracellular levels of cAMP increased by AT. These results suggest that AT inhibits endothelial cell activation by, at least in some part, inhibiting physical interaction of NF-κB with cAMP/p300 by increasing in intracellular levels of cAMP in endothelial cells." @default.
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- W2018360947 date "2003-08-01" @default.
- W2018360947 modified "2023-10-17" @default.
- W2018360947 title "Inhibition by antithrombin of cytokine-induced endothelial cell activation in vitro" @default.
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- W2018360947 doi "https://doi.org/10.1016/s0531-5131(03)00650-2" @default.
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