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CPOX — EPHB2

Text-mined interactions from Literome

Vartiainen et al., J Neurochem 2001 (Hypoxia, Brain) : However, both COX inhibitors induced activation of extracellular signal regulated kinase ( ERK ) in neurones and phosphorylation of heavy molecular weight neurofilaments, cytoskeletal substrates of ERK
Pillinger et al., J Immunol 2003 : Addition of exogenous PGE ( 1 ) or PGE ( 2 ) inhibited MMP-1, reversed the effects of COX inhibitors, and inhibited ERK activation, suggesting that COX-2 activity tonically inhibits MMP-1 production via ERK inhibition by E PGs ... Moreover, COX inhibition sufficient to reduce PGE levels increased ERK activity
Gao et al., Int J Oncol 2005 (Endometrial Neoplasms) : ERK1/2 activation or phosphorylation is responsible for increased cyclooxygenase-2 (COX-2) protein expression in some cancer cells treated with selective COX-2 inhibitor NS398
Clarkin et al., J Cell Physiol 2008 : In ECs, VEGF promoted early ERK1/2 activation, late cyclooxygenase-2 (COX-2) protein induction , and release of 6-keto-PGF1alpha
Sales et al., Mol Cell Endocrinol 2008 (Adenocarcinoma...) : Using chemical inhibitors of intracellular signaling pathways, reporter gene assays and quantitative RT-PCR analysis, we show that PGE ( 2 ) and PGF ( 2alpha ) can mobilize inositol 1,4,5-trisphosphate, induce ERK1/2 phosphorylation via the phospholipase Cbeta-protein kinase A-epidermal growth factor receptor pathway and induce cyclooxygenase-2 (COX-2) expression via the FP receptor
Matsuoka et al., Br J Cancer 2010 (Carcinoma...) : The data suggest that invasion and phosphorylation of ERK were dependent on COX
Chen et al., PloS one 2012 (Inflammation...) : Surprisingly, COX-2 expression in proliferative cells was not blocked by PKCd or ERK1/2 inhibitors due to intrinsic inhibition of PKCd and ERK1/2 in proliferative cells
Lin et al., J Cell Biochem 2013 (MAP Kinase Signaling System...) : In summary, resveratrol and ceramide converge on an endocytosis requiring, ERK1/2 dependent signal transduction pathway and induction of COX-expression as an essential molecular antecedent for subsequent p53 dependent apoptosis