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FGF2 — JUN

Text-mined interactions from Literome

Mohan et al., J Biol Chem 2000 (Neovascularization, Pathologic) : Using cultured corneal cells, we show that FGF-2 stimulates DNA binding activity of transcription factor AP-1 but not NF-kappaB and that AP-1 stimulation is inhibited by curcuminoids
Varghese et al., Endocrinology 2000 : bFGF stimulated the binding of nuclear factors to the collagenase AP-1 site by 3- to 4-fold, as determined by electrophoretic mobility shift assays
Finlay et al., J Biol Chem 2000 : Transforming growth factor-beta 1-induced activation of the ERK pathway/activator protein-1 in human lung fibroblasts requires the autocrine induction of basic fibroblast growth factor
Xu et al., Dev Dyn 2000 : We found that basal and FGF regulated activator protein 1 (AP-1) activity in Xenopus embryo is markedly reduced by treatment of trichostatin A (TSA), a specific inhibitor of HDAC
Schwarz et al., J Immunol 2001 (Inflammation) : This was associated with constitutive induction of the proinflammatory NF-kappaB dependent cytokines IL-1beta, IL-6, and TNF-alpha, and chemokines monocyte chemoattractant protein-1 and IL-8, as well as the AP-1 dependent basic fibroblast growth factor
Yasui et al., Digestion 2004 : FGF-2 induced AP-1-DNA binding activity, and the c-Jun/AP-1 inhibitor curcumin attenuated the FGF-2 induced MMP-1, -3 and TIMP-1 mRNA expression
Cuevas et al., Oncogene 2005 : Both FGF-2 and phorbol ester-inducible urokinase-type plasminogen activator ( uPA ) expression requires AP-1 binding to an enhancer element in the uPA promoter, and we have previously shown that FGF-2 or PMA induction of uPA expression is strongly dependent on MEKK1
Hortala et al., Int J Cancer 2005 (Pancreatic Neoplasms) : In addition, the MEK inhibitor PD98059 reduced the 24 kDa FGF-2 dependent c-Jun level
Wu et al., Mol Cell Biol 2007 : Fibroblast growth factor 2 (FGF-2) and cortisol induced AP-1 and GR occupancy, respectively, at a Notch4 promoter composite response element consisting of an imperfect half-glucocorticoid response element and an AP-1 motif, which mediated signal dependent activation
Torres et al., Cell Tissue Res 2007 : Distribution of cells expressing Jun and Fos proteins and synthesizing DNA in the adrenal cortex of hypophysectomized rats : regulation by ACTH and FGF2 ... The effects of adrenocorticotropic hormone ( ACTH ) and fibroblast growth factor 2 (FGF2) on Fos and Jun protein expression were investigated, and DNA synthesis was assessed by using bromodeoxyuridine ( BrdU ) incorporation
Yang et al., J Biol Chem 2008 (MAP Kinase Signaling System) : Lastly, we examined the role of the immediate-early transcription factors AP-1 and NF-kappaB and have found that phospholipase C-gamma dependent c-Jun and ERK dependent c-fos, but not the NF-kappaB, are strongly activated by bFGF , which in turn regulates the neuronal differentiation of BMSCs
Ahn et al., FEBS Lett 2009 : We demonstrated that FGF2 induces the transient activation of c-Jun N-terminal kinase (JNK) , but not extracellular signal regulated protein kinase or p38 protein kinase
Weber et al., J Invest Dermatol 2010 (MAP Kinase Signaling System...) : In premalignant JB6 cells, bFGF stimulation ( 1 ) increases cellular phospho-ERK and phospho-c-Jun levels, ( 2 ) increases serum dependent cell proliferation, ( 3 ) induces an apparent epithelial-to-mesenchymal transition, and ( 4 ) induces the persistent nuclear-cytosolic oscillation of an ERK1-green fluorescent protein ( ERK1-GFP ) chimera
Li et al., J Oral Sci 2010 (Breast Neoplasms) : Gel mobility shift analyses showed that FGF2 increased the binding of AP1 and CRE2
Nowakowski et al., Ginekol Pol 2012 (Disease Models, Animal...) : AP-1 is induced by extracellular-signal regulated kinases ( ERK 1/2 ) through the activation of basic fibroblast growth factor (bFGF)
Bolego et al., Br J Pharmacol 1997 : 4. Both alpha, beta-meATP and bFGF rapidly and transiently induced the nuclear accumulation of Fos and Jun
Houle et al., Exp Neurol 1998 (Chronic Disease...) : After 8 weeks, c-Jun expression approached baseline levels ; however, removal of scar tissue, with subsequent secondary injury, caused an upregulation of c-Jun expression in both RN and VST neurons, which could be enhanced by CNTF, but not FGF2 , treatment