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Phosphorylation and action of the immunomodulator FTY720 inhibits vascular endothelial cell growth factor-induced vascular permeability.
Vascular endothelial cell adherens junction assembly and morphogenesis induced by sphingosine-1-phosphate.
HDL-bound sphingosine 1-phosphate acts as a biased agonist for the endothelial cell receptor S1P1 to limit vascular inflammation.
Platelet and Erythrocyte Sources of S1P Are Redundant for Vascular Development and Homeostasis, but Both Rendered Essential After Plasma S1P Depletion in Anaphylactic Shock.
An engineered S1P chaperone attenuates hypertension and ischemic injury.
Sphingosine 1-Phosphate Receptor 1 Signaling Maintains Endothelial Cell Barrier Function and Protects Against Immune Complex-Induced Vascular Injury.
Lysolipid receptor cross-talk regulates lymphatic endothelial junctions in lymph nodes.
Induction of cyclooxygenase-2 by interleukin-1 alpha. Evidence for post-transcriptional regulation.
An abundant transcript induced in differentiating human endothelial cells encodes a polypeptide with structural similarities to G-protein-coupled receptors.
Cyclooxygenase gene expression is down-regulated by heparin-binding (acidic fibroblast) growth factor-1 in human endothelial cells.
The immediate-early gene product MAD-3/EDG-3/IkappaB alpha is an endogenous modulator of fibroblast growth factor-1 (FGF-1) dependent human endothelial cell growth.
Cyclooxygenase is an immediate-early gene induced by interleukin-1 in human endothelial cells.
Human cyclooxygenase-2 cDNA.
Recovery of prostacyclin synthesis in human vascular endothelial cells following intermittent or continuous exposure to indomethacin.
The inducible G protein-coupled receptor edg-1 signals via the G(i)/mitogen-activated protein kinase pathway.