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FGF2 — RAC1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: RAC1 → FGF2 (increases, FGF2 Activity)
  Evidence: FGF2 [50] and FGF8b [17] can enhance endothelial cell reorganization onMatrigel.The process requires the activation of the proteolytic machinery, including type IV collagenase(s) and TIMPs production [51] as well as uPA and PAI-1 upregulation [52], a6b1 integrin receptor engagement [53], PECAM-1 [54], and activation of the small GTPase Rac [55].

Text-mined interactions from Literome

Chotani et al., J Biol Chem 2000 : Ras and Rac1 also activated the FGF2 promoter
Jackson et al., Mol Endocrinol 2003 (MAP Kinase Signaling System...) : Moreover, expression of dominant negative Rac also attenuated FGF-2 and FGF-4 stimulation of MAPK ( ERK )
Maddala et al., Molecular vision 2003 : Rac GTPase activation, in contrast, was significantly enhanced in response to only EGF or b-FGF
Shin et al., J Biol Chem 2004 : Basic fibroblast growth factor stimulates activation of Rac1 through a p85 betaPIX phosphorylation dependent pathway ... A GST-PBD binding assay reveals that Rac1 is activated in a dose- and time dependent manner in PC12 cells in response to bFGF ... Expression of mutant PIX markedly inhibits both bFGF- and nerve growth factor (NGF) induced activation of Rac1 , indicating that phosphorylation of p85 betaPIX is responsible for activation of this G protein ... Our results provide evidence that bFGF- and NGF induced phosphorylation of p85 betaPIX mediates Rac1 activation, which in turn regulates cytoskeletal reorganization at growth cones, but not translocation of the PIX complex
Fera et al., J Biol Chem 2004 : For cells on collagen, the immediate activation of Rac1 by FGF-2 was followed by a sustained wave of Rac1 activation that was inhibited when cleavage of the collagen triple helix was prevented and also by blockade of alpha(v)beta(3) integrin
Tkachenko et al., J Cell Sci 2004 : FGF2 and syndecan-4 but not dextran endocytosis were blocked by the dominant negative Rac1 while amiloride and the dominant negative Cdc42 blocked internalization of dextran in addition to FGF2 and syndecan-4
Park et al., J Neurochem 2007 : Transient transfection of kinase-inactive MEKK7 or chemical inhibitors of JNK significantly decreased the activation of Rac1 by FGF
Vogt et al., Cell Signal 2007 : The switch from Rac1 to RhoA activation in H10 cells was controlled by fibroblast growth factor-2 (FGF-2) , lowering the expression of RGS3L
Yan et al., Mol Cell Biol 2008 : Finally, the activation levels of extracellular signal regulated kinase ( ERK ), p38, and Rac , which are important signaling molecules in angiogenesis, were all reduced in response to FGF2 when either of the Rap1 proteins was depleted
Elfenbein et al., J Cell Biol 2009 : Thus, FGF2 induced Rac1 activation depends on the suppression of RhoG by a previously uncharacterized ternary S4-synectin-RhoGDI1 protein complex and activation via PKCalpha
Kanazawa et al., PloS one 2010 (MAP Kinase Signaling System) : bFGF activated RhoA, Rac1 , PI3-kinase, and JNK in cultured fibroblasts
Lee et al., Invest Ophthalmol Vis Sci 2011 : FGF-2 activated Rac1 through Akt, and Rac1 inhibitor greatly inhibited the FGF-2 stimulated cell proliferation
Huang et al., Neurobiol Dis 2012 (Cerebral Hemorrhage, Traumatic) : Exogenous FGF2 increased activated FGFR, Akt, and Rac1 but reduced activated RhoA protein expression at 72 h after cICH ( p < 0.05, compared to vehicle ), which was reversed by FGFR and PI3K inhibition
Kovacevic et al., EMBO J 2012 : Furthermore, NOSTRIN is required for fibroblast growth factor 2 dependent activation of Rac1 in primary endothelial cells and the angiogenic response to fibroblast growth factor 2 in the in vivo matrigel plug assay