Gene interactions and pathways from curated databases and text-mining

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PRKAR1A — PTGS2

Text-mined interactions from Literome

Zhou et al., J Clin Endocrinol Metab 1999 : Inhibition of PKA activity by cotreatment with isoquinoline-sulfonamide ( H-89 ) prevented hCG from increasing COX-2 protein levels
Tamura et al., J Clin Endocrinol Metab 2002 : COX-2 mRNA, protein, and PGE ( 2 ) levels in IL-1beta treated ESC were decreased by a PKA inhibitor, a nuclear factor ( NF-kappaB ) inhibitor, and an ERK1/2 inhibitor, but not by a p38 MAPK inhibitor or a PKC inhibitor, suggesting the possible involvement of PKA , NF-kappaB, and/or the ERK1/2 signaling pathway ( s ) in IL-1beta mediated COX-2 gene induction in ESC
Tortora et al., Clin Cancer Res 2003 (Neovascularization, Pathologic) : COX-2 expression can be induced by EGFR activation and is regulated by cAMP and PKA
Sakuma et al., Bone 2004 : Treatment with specific inhibitors indicated that PGE ( 2 ), EP2A, and EP4A induced COX-2 expression largely through protein kinase A (PKA)
Choudhary et al., Biochem Biophys Res Commun 2004 : In contrast, PKA inhibitors, used at doses that inhibited forskolin stimulated luciferase activity by 90 %, reduced [ Ca(+2) ] ( e ) -stimulated COX-2 mRNA expression and promoter activity by 80-90 %
Park et al., Biochem Biophys Res Commun 2007 : PKA , ERK, and p38 MAPK pathways regulate COX-2 mRNA expression induced by rolipram, in which PKA is a central regulator of the ERK and p38 MAPK pathways
Simeone et al., Int J Oncol 2007 (Breast Neoplasms...) : Protein kinase A (PKA) and protein kinase C ( PKC ) are activated by COX-2 and are involved in IL-8 regulation
Misior et al., Am J Respir Cell Mol Biol 2009 : Recent studies have suggested that GCs render agents of inflammation such as IL-1 beta and TNF-alpha mitogenic to ASM, via suppression of ( antimitogenic ) induced cyclooxygenase-2 dependent PKA activity
Friis et al., J Am Soc Nephrol 2009 : Taken together, our results show that a 5 to 7 % decrease in extracellular tonicity leads to AQP1 mediated water influx in JG cells, PLA(2)/COX-2 mediated prostaglandin dependent formation of cAMP, and activation of PKA , which promotes exocytosis of renin
Lee et al., Allergy, asthma & immunology research 2013 : LPS induced COX-2 expression in RAW 264.7 macrophages was enhanced by exogenous PGE2 or cyclic AMP ( cAMP ) analogue and was suppressed by a COX inhibitor ( indomethacin ), a protein kinase A (PKA) inhibitor ( KT5720 ), and A kinase anchoring protein ( AKAP ) disruptors ( Ht31 and RIAD )
Warnock et al., J Cell Physiol 1995 (Second Messenger Systems) : The addition of various PKC inhibitors also blocked the IL-1 beta induction of PGHS-2 mRNA but did not alter PGHS-1 mRNA expression ; inhibitors of protein kinase A (PKA) or tyrosine kinase ( TK ) had only a limited effect on IL-1 beta induced PGHS-2 mRNA expression
Tsai et al., Endocrinology 1996 : PGHS-2 was acutely ( < 12 h ) increased by PKA , and to a lesser extent by PKC ... Temporal expression of FP receptor mRNA is not consistent with the involvement of FP receptor in ovulation and suggests that PKA stimulates PGHS-2 and FP receptor mRNA by distinct mechanisms