Pathways - manually collected, often from reviews:
OpenBEL Selventa BEL large corpus:
RAC1
→
FLT1
(increases, FLT1 Activity, RAC1 Activity)
Zeng et al., J Biol Chem 2002* Evidence: Recently, it has been shown that KDR is responsible for VPF/VEGF-stimulated endothelial cell (EC) proliferation and migration, whereas Flt-1 activation down-modulates KDR-mediated EC proliferation. Although KDR-mediated EC proliferation and migration have been extensively studied, much less is known about Flt-1-mediated antiproliferation. Here, we demonstrate that Flt-1-mediated antiproliferative activity can be blocked completely by the dominant negative mutant of CDC42 (CDC42-17N) and partiall...
OpenBEL Selventa BEL large corpus:
RAC1
→
FLT1
(increases, FLT1 Activity, RAC1 Activity)
Zeng et al., J Biol Chem 2002* Evidence: Using the chimeric-receptor EGLT in which the extracellular domain of epidermal growth factor receptor was fused to the transmembrane and intracellular domains of Flt-1, we also demonstrate that CDC42 and Rac1 are activated by EGLT. Previously, we showed that phosphatidylinositol 3-kinase is required for Flt-1-mediated antiproliferative activity, but phospholipase C is not required.