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IL6 — PRKAR2A

Text-mined interactions from Literome

Murakami et al., J Periodontal Res 2000 (Periodontitis) : Adenosine induced IL-6 production was suppressed by protein kinase A (PKA) inhibitor, H89, indicating that cAMP/PKA pathway is involved in the induction
Ding et al., Cytokine 2000 : Both inhibitors and activators for PKA and G-protein as well as IL-10 had no effects on IL-6 expression
Kiriyama et al., Endocrinology 2001 : Furthermore, calcitonin induced IL-6 production was completely suppressed by H-89 ( PKA inhibitor ) or GF109203X ( PKC inhibitor ), indicating that the activation of both PKA and PKC is necessary for calcitonin induced IL-6 production
Tsingotjidou et al., Bone 2002 : PTH induces IL-6 through PKA activation, whereas fluprostenol induces IL-6 through PKC activation
Ha et al., J Leukoc Biol 2005 : Further characterization of the response to PSG17 indicated that cyclic adenosine monophosphate dependent protein kinase A (PKA) is involved in the up-regulation of IL-10 and IL-6 , and it is not required for the induction of TGF-beta(1)
Obara et al., Mol Pharmacol 2005 (Astrocytoma) : Furthermore, both CREB and IL-6 promoter activities were suppressed by SB203580 [ 4- ( 4-fluorophenyl ) -2- ( 4-methylsulfinylphenyl ) -5- ( 4-pyridyl ) -1H-imidazole ], a p38 mitogen activated protein kinase ( MAPK ) inhibitor, and H89 [ N- [ 2- ( 4-bromocinnamylamino ) -ethyl ] -5-isoquinoline ], a protein kinase A (PKA) inhibitor, indicating involvements of p38 MAPK and PKA in CREB activation and IL-6 expression
Chen et al., J Immunol 2006 : PGN mediated IL-6 production was inhibited by a nonselective cyclooxygenase (COX) inhibitor ( indomethacin ), a selective COX-2 inhibitor ( NS398 ), a PGE ( 2 ) ( EP2 ) antagonist ( AH6809 ), a PGE ( 4 ) ( EP4 ) antagonist ( AH23848 ), and a protein kinase A (PKA) inhibitor ( KT5720 ), but not by a nonselective NO synthase inhibitor ( N ( G ) -nitro-l-arginine methyl ester ) ... These results suggest that PGN induced IL-6 production involves COX-2 generated PGE ( 2 ), activation of the EP2 and EP4 receptors, cAMP formation, and the activation of PKA , protein kinase C, p38 MAPK, IKKdbeta, kinase alphabeta, p65 phosphorylation, and NF-kappaB
Wang et al., Am J Physiol Cell Physiol 2010 : Simultaneous inhibition of PKA and PI3K reduces IL-6 expression in stimulated chondrocytes well below the basal levels of untreated cells
Ji et al., Liver Transpl 2012 (Disease Models, Animal...) : In vitro, cAMP-PKA activation diminished macrophage tumor necrosis factor a, IL-6 , and IL-12 in an IL-10 dependent manner and prevented necrosis/apoptosis in primary mouse hepatocyte cultures
Ji et al., Hepatology 2013 (Liver Diseases...) : In vitro, PACAP treatment not only diminished macrophage tumor necrosis factor alpha/IL-6/IL-12 levels in a PKA dependent manner, but also prevented necrosis and apoptosis in primary mouse hepatocyte cultures
de Wit et al., Br J Haematol 1994 : Using the human monocytic cell line Mono Mac 6 we studied the involvement of Ca2+, protein kinase A (PKA) , and protein kinase C ( PKC ) dependent pathways in the regulation of M-CSF and IL-6 gene expression
Millet et al., J Bone Miner Res 1998 : Moreover, we show that PGE2 mediated IL-6 induction is prevented by the cAMP antagonist, Rp-cAMP, and the protein kinase A (PKA) inhibitors, KT5720 and H89
Zidovetzki et al., AIDS Res Hum Retroviruses 1998 : Tat induced increase in IL-6 mRNA was abolished in the presence on PK-A inhibitor H-89, demonstrating that activation of PK-A is necessary and sufficient for the increase in IL-6 production by these cells
Zeng et al., J Pharmacol Exp Ther 1998 : Pharmacological agents that increase intracellular concentration of cyclic AMP ( [ cAMP ] i ) mimicked and synergistically enhanced induction of IL-6 secretion by PGE2, whereas inhibitors of protein kinase A (PKA) but not protein kinase C suppressed PGE2 evoked increases in IL-6 secretion, suggesting that cAMP and PKA are the intracellular messengers of the PGE2 effect