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Thrombin-induced autoinhibitory factor, Down syndrome critical region-1, attenuates NFAT-dependent vascular cell adhesion molecule-1 expression and inflammation in the endothelium.
G protein-coupled receptor Ca2+-linked mitochondrial reactive oxygen species are essential for endothelial/leukocyte adherence.
Thrombin stimulation of the vascular cell adhesion molecule-1 promoter in endothelial cells is mediated by tandem nuclear factor-kappa B and GATA motifs.
Thrombin and phenotypic modulation of the endothelium.
Priming effect of homocysteine on inducible vascular cell adhesion molecule-1 expression in endothelial cells.
Vascular endothelial growth factor- and thrombin-induced termination factor, Down syndrome critical region-1, attenuates endothelial cell proliferation and angiogenesis.
Thrombin stimulation of vascular adhesion molecule-1 in endothelial cells is mediated by protein kinase C (PKC)-delta-NF-kappa B and PKC-zeta-GATA signaling pathways.
Thrombin, TNF-alpha, and LPS exert overlapping but nonidentical effects on gene expression in endothelial cells and vascular smooth muscle cells.
Preconditioning of primary human endothelial cells with inflammatory mediators alters the "set point" of the cell.
Thrombin downregulates thrombomodulin expression and activity in primary human endothelial cells.
Vascular endothelial growth factor activation of endothelial cells is mediated by early growth response-3.
The proximal serum response element in the Egr-1 promoter mediates response to thrombin in primary human endothelial cells.
MOLECULAR BASIS OF CARDIAC-SPECIFIC HEMOSTASIS-COLLABORA
TRANSCRIPTIONAL CONTROL OF CARDIAC-SPECIFIC HEMOSTASIS