◀ Back to FGF2

FGF2 — IFI44

Text-mined interactions from Literome

Hata et al., Diabetes 1999 : Basic fibroblast growth factor induces expression of VEGF receptor KDR through a protein kinase C and p44/p42 mitogen activated protein kinase dependent pathway
Beer et al., J Biol Chem 2000 : Despite their apparently similar but low affinities, FGF-10 but not FGF-7 induced the activation of p44/42 mitogen activated protein kinase in FGFR1-IIIb expressing L6 myoblasts and stimulated mitogenesis in these cells, demonstrating that this new receptor variant is a functional transmembrane receptor for FGF-10
Zhang et al., Hypertens Res 2000 : 1 ) bFGF ( 20 ng/ml ) significantly activated p42/p44 MAPKs with a peak time of 5-15 min, which was maintained for 3 h. PD98059 ( 100 nM-10 microM ), a specific inhibitor of MAPK kinase, inhibited bFGF induced p42/p44 MAPKs activation in a dose dependent manner ... Amlodipine, which could inhibit bFGF induced human VSMC proliferation, inhibited both short-term and sustained p42/p44 MAPKs activation by bFGF , suggesting that bFGF induced VSMC proliferation may be related to p42/p44 MAPKs activation, and that the antiproliferative effect of amlodipine may be related to its inhibition of p42/p44 MAPKs activation
Delehedde et al., Biochem J 2002 : Fibroblast growth factor-2 binds to small heparin derived oligosaccharides and stimulates a sustained phosphorylation of p42/44 mitogen activated protein kinase and proliferation of rat mammary fibroblasts
Ghiselli et al., Arterioscler Thromb Vasc Biol 2003 : FGF mediated phosphorylation of p42/p44 mitogen activated protein kinase ( MAPK ) c-Raf, MAP kinase kinase kinase, MEK1/2 MAP kinase, kinase, stress activated protein kinase/c-Jun-NH2-terminal kinase, and p38 MAPK were variably reduced by ethanol
Chaturvedi et al., Endocrinology 2005 : In both of these cell populations, bFGF also increased phosphorylation of MAPK p44/42 ... U0126, an inhibitor of MAPK p44/42, blocked the bFGF induced activation of MAPK p44/42 as well as the bFGF induced cell proliferation of enriched lactotropes and PR1 cells ... Treatment of PR1 cells with bFGF increased the activity of Ras p21, whereas overexpression of a dominant negative mutant of Ras p21 abrogated the bFGF induced activation of MAPK p44/42 in these cells ... Furthermore, the Src kinase inhibitor PP1 suppressed bFGF induced activation of MAPK p44/42 in both enriched lactotropes and PR1 cells ... On the other hand, the bFGF induced activation of MAPK p44/42 in enriched lactotropes and PR1 cells was not affected by protein kinase C inhibitors ... These data suggest that bFGF induction of lactotropic cell proliferation is possibly mediated by activation of Src kinase, Ras p21, and MAPK p44/42
Yasuda et al., Biochem Biophys Res Commun 2005 : We previously reported that basic fibroblast growth factor ( FGF-2 ) activates stress activated protein kinase/c-Jun N-terminal kinase ( SAPK/JNK ) and p44/p42 mitogen activated protein ( MAP ) kinase resulting in the stimulation of vascular endothelial growth factor ( VEGF ) release in osteoblast-like MC3T3-E1 cells and that FGF-2 activated p38 MAP kinase negatively regulates the VEGF release
Pan et al., J Pharmacol Exp Ther 2005 (Neoplasms...) : YC-1 inhibited VEGF- and bFGF induced p42/p44 mitogen activated protein kinase and Akt phosphorylation as well as protein kinase C alpha translocation using Western blot analysis
Chaturvedi et al., J Pharmacol Exp Ther 2005 (MAP Kinase Signaling System) : Role of protein kinase C-Ras-MAPK p44/42 in ethanol and transforming growth factor-beta3 induced basic fibroblast growth factor release from folliculostellate cells
de Alvaro et al., Mol Biol Cell 2005 : When C2C12 cells were stably transfected with a Sprouty-2 ( Y55F ) mutant defective in inhibiting p44/p42-MAPK activation by FGF , myoblasts in the presence of FGF continue to grow and completely fail to form myotubes
Hanai et al., Life Sci 2006 : We previously reported that basic fibroblast growth factor ( FGF-2 ) activates stress activated protein kinase/c-Jun N-terminal kinase ( SAPK/JNK ) and p44/p42 mitogen activated protein ( MAP ) kinase resulting in the stimulation of vascular endothelial growth factor ( VEGF ) release in osteoblast-like MC3T3-E1 cells
Takai et al., Mol Cell Endocrinol 2007 : We previously reported that basic fibroblast growth factor ( FGF-2 ) activates stress activated protein kinase/c-Jun N-terminal kinase ( SAPK/JNK ) and p44/p42 mitogen activated protein ( MAP ) kinase, resulting in the release of vascular endothelial growth factor ( VEGF ) in osteoblast-like MC3T3-E1 cells
Seo et al., Microvasc Res 2008 (MAP Kinase Signaling System) : We also show that TIMP-2 inhibition of FGF-2 induced p42/44(MAPK) activation and cell proliferation is associated with TIMP-2 binding to integrin alpha3beta1 on endothelial cell surfaces, as demonstrated by use of anti-integrin alpha3 or beta1 blocking antibodies, or disruption of integrin alpha3 expression by siRNA