Gene interactions and pathways from curated databases and text-mining

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PTGS2 — RNF19A

Text-mined interactions from Literome

McGinty et al., Biochem J 2000 : Similarly, activation of JNK by Ad-MKK7D and p38-MAPK by Ad-MKK3bE/Ad-MKK6bE resulted in the increased expression of PGHS-2
Kulkarni et al., Clin Cancer Res 2001 (Adenocarcinoma...) : The induction of COX-2 by EGF was suppressed by inhibitors of tyrosine kinase activity, phosphatidylinositol 3-kinase, mitogen activated protein kinase kinase, and p38 mitogen activated protein kinase ... Moreover, overexpressing dominant negative forms of extracellular signal regulated kinase 1, c-Jun NH2-terminal kinase, p38 , and c-Jun blocked EGF mediated induction of COX-2 promoter activity
Kim et al., Dig Dis Sci 2001 : An NF-kappaB inhibitor ( pyrrolidine dithiocarbamate ), a MAP kinase ( MEK ) inhibitor ( PD98059 ), and a p38 MAP kinase inhibitor ( SB203580 ) significantly suppressed the COX-2 gene transcription and PGE2 synthesis in the neutrophils
Park et al., Mol Pharmacol 2002 : Moreover, IL-1 beta stimulation of the cells caused the phosphorylation of p38 and extracellular signal regulated kinase ( ERK ), and IL-1 beta induced COX-2 expression was inhibited by the pretreatment of WISH cells with a p38 inhibitor, in contrast ERK upstream inhibitor had no effect
Nagano et al., Int Immunol 2002 : Taken together, these results suggest that both ERK and p38 ( MAPK ) pathways are involved in LPS induced COX-2 expression and PGE ( 2 ) production in neutrophils, and IL-10 and IL-4 inhibit neutrophil prostanoid synthesis by down regulating the activation of p38 ( MAPK )
Degousee et al., Circ Res 2003 (MAP Kinase Signaling System) : These results provide direct evidence that MKK6 mediated p38 MAPK activation is necessary for interleukin-1beta induced cardiac myocyte COX-2 gene expression and PGE2 biosynthesis in vitro and is sufficient for COX-2 gene expression by cardiac myocytes in vitro and in vivo
Ho et al., Br J Pharmacol 2004 (Inflammation) : The selective p38 MAPK inhibitor, SB203580, inhibited the promoter activities of iNOS and COX-2 rather than that of TNF-alpha
Yamaguchi et al., Arterioscler Thromb Vasc Biol 2004 (Diabetes Mellitus) : PDGF-BB induced p38 phosphorylation also regulated cell growth, cyclooxygenase-2 levels, and arachidonic acid release, but not apoptosis
Gutiérrez-Venegas et al., Life Sci 2005 : However, p38 inhibition only partially blocked COX-2 expression and PGE2 synthesis
Kucknoor et al., Cell Microbiol 2005 : Data suggest that p38 mitogen activated protein ( MAP ) kinase and tyrosine kinases play a role in COX-2 induction
Jang et al., Free Radic Biol Med 2005 (MAP Kinase Signaling System) : Pharmacologic inhibition of extracellular signal regulated kinase ( ERK ) and p38 mitogen activated protein kinase ( p38 MAPK ) and dominant negative mutation of both enzymes suppressed not only Abeta induced NF-kappaB transactivation but also COX-2 expression and PGE ( 2 ) production
Shafer et al., Biochim Biophys Acta 2005 : These results indicate that activation of p38MAPK signaling is sufficient for COX-2 expression in IEC-18 cells
Ulivi et al., J Cell Biochem 2008 (Inflammation) : p38/NF-kB dependent expression of COX-2 during differentiation and inflammatory response of chondrocytes
Ulivi et al., J Cell Physiol 2008 (Inflammation) : ( 4 ) p38 is involved in the PPARgamma mediated induction of COX-2
Park et al., J Dent Res 2010 : Studies on the intra-cellular signaling pathways revealed that p38 activation is required for the synergistic activation of Cox-2 by TLR2 and histamine
Husvik et al., Eur J Oral Sci 2009 (Carcinoma, Squamous Cell...) : Thus, JNK negatively regulated EGF induced extracellular signal regulated kinase 1/2 and/or p38 mediated COX-2 transcription, presumably through activating an unidentified phosphatase
Cho et al., Mol Immunol 2011 : Pharmacologic inhibitors of ERK and p38 mitogen activated protein kinases inhibited the COX-2 upregulation
Zhu et al., Acta Pharmacol Sin 2012 (MAP Kinase Signaling System) : Aldosterone treatment significantly increased the expression of Cox-2 and IL-6 and activation of p38MAPK and NF-?B
Guan et al., J Biol Chem 1998 : We reported previously that IL-1beta rapidly activates the c-Jun NH2-terminal/stress activated protein kinases ( JNK/SAPK ) and p38 mitogen activated protein kinase ( MAPK ) and also induces Cox-2 expression and prostaglandin E2 ( PGE2 ) production
Dean et al., J Biol Chem 1999 : p38 mitogen activated protein kinase regulates cyclooxygenase-2 mRNA stability and transcription in lipopolysaccharide treated human monocytes