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IL6 — PRKACB
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