Gene interactions and pathways from curated databases and text-mining

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EPHB2 — FOSL1

Text-mined interactions from Literome

Young et al., Mol Cell Biol 2002 (Cell Transformation, Neoplastic) : The results establish that the transactivation domain of Fra-1 can be activated, that activation of Fra-1 is ERK dependent , and that a putative ERK phosphorylation site must be intact for activation to occur ... These observations suggest that ERK dependent activation of Fra-1 is required for AP-1 transactivation in JB6 cells
Ramos-Nino et al., Cancer Res 2002 (Cell Transformation, Neoplastic...) : Mesothelial cell transformation requires increased AP-1 binding activity and ERK dependent Fra-1 expression ... In summary, we demonstrate that ERK dependent Fra-1 is elevated in AP-1 complexes in response to asbestos fibers and is critical to the transformation of mesothelial cells
Liu et al., Am J Physiol Lung Cell Mol Physiol 2003 : Blocking ERK1/2 activation by MEK1/2 inhibitors ( PD-98059 or U-0126 ) diminishes HB-EGF induced Fra-1 accumulation and subsequent downregulation of elastin mRNA
Vial et al., Cancer Cell 2003 (Colonic Neoplasms...) : The Fos family member Fra-1 is expressed in an ERK dependent manner
Zhang et al., Am J Physiol Lung Cell Mol Physiol 2004 (MAP Kinase Signaling System) : Furthermore, inhibitors of ERK1/2 , JNK1, and p38 mitogen activated protein kinases ( MAPKs ) significantly suppressed DEP stimulated fra-1 transcription, suggesting their involvement in the induction process
Vial et al., J Cell Sci 2003 (Colonic Neoplasms) : We show that c-JUN and FRA-1 expression is dependent on ERK activity and that different thresholds of ERK activity control the expression of FRA-1
Marek et al., J Cell Physiol 2004 : Like NFLC, induction of urokinase plasminogen activator (uPAR), transin/matrix metalloproteinase 3 (MMP3), Fra-1 and transforming growth factor beta 1 ( TGF beta 1 ) required collaborative ERK and JNK signaling while the increased expression of cortexin, rat collapsin response mediator protein 4 ( rCRMP4 ), rat growth and transformation dependent protein ( RGT ), and synapsin II required neither mitogen activated protein kinase ( MAPK ) pathway
Zhang et al., Am J Respir Cell Mol Biol 2005 : Furthermore, treatment of cells with GM6001, which inhibits matrix metalloproteinase activity, significantly suppressed CS-stimulated EGF shedding, EGFR and ERK kinase phosphorylation, and subsequent fra-1 induction
Hoffmann et al., J Biol Chem 2005 : Additional experiments reveal that, in conjunction with p65 NF-kappaB, the MEK1-ERK dependent synthesis of c-Fos and Fra-1 serves to adjust the overall expression level of IL-8 in response to two of its physiological inducers, IL-1 and epidermal growth factor
Hamdi et al., DNA repair 2008 (Brain Neoplasms...) : Furthermore, JNK but not ERK is required for ATF3 induction, and both ERK and JNK are necessary for post-transcriptional induction of Fra1 in response to cisplatin or UV
Julien et al., J Bone Miner Res 2009 : U0126 ( MEK1/2 inhibitor ) suppressed Pi-stimulated MGP and Fra-1 expression, indicating that ERK1/2 is required for Pi-dependent regulation of MGP and Fra-1
Camalier et al., Cancer prevention research (Philadelphia, Pa.) 2010 (Cell Transformation, Neoplastic...) : Supplementation of medium with phosphate increased anchorage independent transformation and proliferation of BALB/c mouse JB6 epidermal cells, activation of N-ras, ERK1/2 , and activator protein-1, and increased gene expression of Fra-1 , COX-2, and osteopontin in a dose dependent manner
Lan et al., J Virol 2012 (Epstein-Barr Virus Infections...) : Notably, LMP2A promoted invasion of NPC cells was blocked when MMP9 expression, Fra-1 induction , or ERK1/2 activation was inhibited
Treinies et al., Mol Cell Biol 1999 : Treatment of Ras transformed cells with the MEK inhibitor PD098059 blocks expression of Fra-1 and Fra-2, showing that in Ras transformation ERK signalling is responsible for Fra-1 and Fra-2 expression