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PRKAR1A — TNF

Text-mined interactions from Literome

Nakamura et al., J Am Soc Nephrol 2001 : However, inhibition of MAPK ( p42/p44 ) and TNF-alpha promoter activity was partially prevented by the cAMP-protein kinase (PKA) inhibitors, H-89 ( 5 x 10 ( -6 ) M ) and KT5720 ( 10 ( -5 ) M ), whereas the suppression of p38 MAPK or NF-kappa B ( p50 ) was not blocked by these inhibitors ... It is likely that cAMP-PKA and MAPK ( p42/p44, p38 ) may play a critical role in the regulation of the Stx-2 induced TNF-alpha transcription via beta(2)-adrenoceptor activation
Yoon et al., J Biol Chem 2003 : Taken together, our results indicate that stimulation of PKA by alpha-MSH causes inhibition of LPS induced activation of p38 kinase and NF kappa B to block TNF-alpha production
Chen et al., Endocrinology 1992 : TNF alpha increased cAMP and also increased relative PKA and PKC activity in 1-40 min. Phorbol myristate acetate ( PMA ), an activator of PKC, increased [ 3H ] thymidine incorporation and DNA content
Aronoff et al., J Immunol 2005 : By contrast, activation of PKA , but not Epac-1, suppressed AM production of leukotriene B ( 4 ) and TNF-alpha , whereas stimulation of either PKA or Epac-1 inhibited AM bactericidal activity and H ( 2 ) O ( 2 ) production
Zhao et al., Cell Immunol 2005 (MAP Kinase Signaling System) : Although gAd partially increased cAMP concentration and PKA activity, it directly reduced leptin induced ERK1/2 and p38 MAPK phosphorylation thus inhibiting TNF-alpha production
Hichami et al., Mediators Inflamm 1996 : We investigated the effects of specific inhibitors of cAMP dependent protein kinase (PKA) and cGMP dependent protein kinase ( PKG ) on the inhibitory activity of phosphodiesterase ( PDE ) type 4 inhibitors and of the cell permeable analogue of cAMP, db-cAMP on LPS induced TNF-alpha release from human mononuclear cells
Beck et al., Biochem Pharmacol 2009 (Inflammation) : Although H89 can inhibit both MSK1 and PKA, TNF does not activate PKA ( EC 2.7.11.11 ) and as such PKA inhibition does not mediate H89 instigated repression of TNF stimulated gene expression
Wall et al., Science signaling 2009 (Inflammation...) : Suppression of LPS induced TNF-alpha production in macrophages by cAMP is mediated by PKA-AKAP95-p105
Kim et al., J Biol Chem 2011 : AKAP10 also mediated PGE ( 2 ) potentiation of the expression of cytokines IL-10 and IL-6, whereas PGE ( 2 ) suppression of TNF-a was mediated by AKAP8 anchored PKA-RII
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
Scheurich et al., J Exp Med 1989 : As activation of PKA does not slow down the degradation rate of TNF-Rs, but rather enhances protein synthesis dependent reexpression of TNF-Rs after transient PKC mediated transmodulation and after tryptic digestion of TNF-Rs, it is concluded that PKA stimulates TNF-R synthesis ... PKA mediated enhancement of TNF-R expression was predominantly observed in normal peripheral blood monocytes and tumor cell lines of myeloid origin ... As in these typical TNF producer cells, the production of TNF is also controlled by PKA and PKC, a regulatory circuit is proposed, by which these two independent signal pathways antagonistically regulate TNF production and, at the receptor level, TNF sensitivity
Seldon et al., Mol Pharmacol 1995 : When PGE2 was used to activate adenylyl cyclase, however, rolipram potentiated cAMP accumulation, PKA activation, and inhibition of TNF-alpha generation