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CREB5 — FGF2

Text-mined interactions from Literome

Hansen et al., Mol Endocrinol 1999 : bFGF stimulation led to phosphorylation of the p38 mitogen activated protein kinase ( MAPK ), and the extracellular signal regulated kinase ( ERK ) MAPK and promoter activation, phosphorylation of CREB , and GAL4-CREB dependent transcription were selectively prevented by a dominant negative Ras-mutant, the p38 MAPK-specific inhibitor SB203580, and the MAP/ERK kinase 1 (MEK1) inhibitor PD098059
Sung et al., J Biol Chem 2001 : Interestingly, bFGF induced CREB phosphorylation and subsequent CRE mediated gene transcription is not likely to be mediated by any of previously known signaling pathways that lead to phosphorylation of CREB, such as mitogen activated protein kinases, protein kinase A, protein kinase C, phosphatidylinositol 3-kinase-p70 ( S6K ), calcium/calmodulin dependent protein kinase, and casein kinase 2
Yang et al., J Biol Chem 2001 (Down Syndrome) : Blockade of Dyrk1 activation significantly inhibits the neurite outgrowth as well as CREB phosphorylation induced by basic fibroblast growth factor
Bayatti et al., J Neurochem 2001 (MAP Kinase Signaling System) : On the other hand, increases in intracellular cAMP levels in cortical astroglia prolonged FGF-2 induced CREB phosphorylation and subsequently potentiated the cAMP response element dependent transcription of the immediate early gene, c-fos ... Moreover, the effects of cAMP on the time-course of FGF-2 dependent CREB phosphorylation were mimicked by PD98059, suggesting that the cAMP induced redirection of FGF-2 signalling is linked to the RAF-MEK-ERK signalling pathway
Tada et al., J Invest Dermatol 2002 : The concomitant presence of endothelin-1, basic fibroblast growth factor , and alpha-melanotropin significantly potentiated CREB phosphorylation
Mattos et al., Mol Cell Endocrinol 2005 (Adrenal Cortex Neoplasms) : We found that FGF2 was mitogenic only in glomerulosa cells and although ACTH did not activate ERK1/2, it did activate CREB protein, indicating efficient transduction of signals initiated in the ACTH receptors of rat adrenocortical cells
Azadi et al., Brain Res 2007 (Disease Models, Animal...) : To shed light on the underlying mechanisms, we studied the effects of 9 days ( starting at postnatal day 2 ) in vitro CNTF+BDNF treatment on the endogenous production of CNTF, BDNF, fibroblast growth factor 2 (FGF2), or the activation of extracellular signal regulated kinase ( ERK ), Akt and cAMP-response-element binding protein ( CREB ) in retinal explants
Ditlevsen et al., Neurochem Int 2008 : For comparison, we also evaluated the role of upstream signalling cascades on fibroblast growth factor 2 (FGF2) mediated phosphorylation of ERK, Akt, and CREB and found that FGF2 required the activity of both FGFR and Src-family kinases for phosphorylation of ERK, Akt, and CREB
Galardo et al., J Endocrinol Invest 2013 : The aim of this study was to investigate if bFGF and IL1ß activate CREB , what signaling pathways may be participating and the possible relationship between CREB activation and the regulation of Sertoli cell function ... MEK inhibitors -- PD98059 and U0126 -- blocked the effect of bFGF on phosphorylated CREB while a p38-MAPK inhibitor -- SB203580 -- blocked the effect of IL1ß on phosphorylated CREB ... The results presented herein suggest that CREB is stimulated in response to bFGF and IL1ß through p42/p44-MAPK and p38-MAPK pathways and that this transcription factor may be partially responsible for the regulation of Sertoli cell function
Tabernero et al., Mol Cell Neurosci 1998 : In contrast, neurotrophins, CNTF, FGF-2 , EGF, and TGF beta induce little or no phosphorylation of CREB despite the fact that receptors for these factors are present on Schwann cells ... In contrast, neurotrophins, CNTF, FGF-2 , EGF, and TGF beta induce little or no phosphorylation of CREB despite the fact that receptors for these factors are present on Schwann cells