◀ Back to IL10
IL10 — PRKACG
Text-mined interactions from Literome
Yang et al., J Immunol 2003
(Glioma) :
However, KT5720, a selective
PKA inhibitor,
reduced neither anti-Fas triggered nor glioma associated
IL-10 expression
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)
Park et al., J Leukoc Biol 2008
:
Inhibition of either ERK1/2 or
PKA activity
prevented gAcrp stimulated CREB phosphorylation, as well as gAcrp stimulated
IL-10 promoter activation
Seo et al., Exp Mol Med 2008
:
Further, we obtained evidence of crosstalk between P2 receptors, in a situation where intracellular Ca ( 2+ ) release and/or cAMP activated
PKA were the main contributors to extracellular ATP- ( or ADP ) -mediated IL-10 expression, and
IL-10 production was
down-regulated by either MRS2179 ( a P2Y ( 1 ) antagonist ) or 5'-AMPS ( a P2Y ( 11 ) antagonist ), indicating that both the P2Y(1) and P2Y(11) receptors are major receptors involved in IL-10 expression
Pongratz et al., Ann Rheum Dis 2012
(Arthritis, Experimental) :
Interleukin 10 (IL-10) producing B cells suppress arthritis and are a potential target of the SNS because ( 1 ) B cells express functional ß ( 2 ) -adrenoceptors ( ß ( 2 ) ARs ) and ( 2 )
IL-10 , at least in monocytes/macrophages, is regulated in a
cAMP/PKA/CREB dependent manner
Lieskovska et al., Parasite Immunol 2012
:
Saliva induced enhancement of
IL-10 was not observed in the
presence of specific inhibitor of
Protein Kinase A (PKA) , H-89, suggesting the involvement of PKA pathway in IL-10 production