PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15946940-6 2005 cAMP response element-binding protein (CREB) is one downstream target of iPLA2 that is required for the transcriptional activation of iNOS in response to virus infection, and consistent with the effects of BEL enantiomers on iNOS expression, (S)-BEL more effectively inhibits EMCV-induced CREB phosphorylation than (R)-BEL in macrophages. Cyclic AMP 0-4 nitric oxide synthase 2 Homo sapiens 134-138 17714696-5 2007 The alpha1-AR stimulation resulted in the activation of phosphoinositide turnover (InsP) via phospholipase C (PLC) involving calcium/calmodulin (CaM) and nitric oxide synthase (NOS) that correlates with the DNA synthesis increment; whereas the inhibition resulted in a decrease of cyclic AMP (cAMP) accumulation via adenylate cyclase inhibition. Cyclic AMP 281-291 nitric oxide synthase 2 Homo sapiens 154-175 17714696-5 2007 The alpha1-AR stimulation resulted in the activation of phosphoinositide turnover (InsP) via phospholipase C (PLC) involving calcium/calmodulin (CaM) and nitric oxide synthase (NOS) that correlates with the DNA synthesis increment; whereas the inhibition resulted in a decrease of cyclic AMP (cAMP) accumulation via adenylate cyclase inhibition. Cyclic AMP 293-297 nitric oxide synthase 2 Homo sapiens 154-175 15946940-6 2005 cAMP response element-binding protein (CREB) is one downstream target of iPLA2 that is required for the transcriptional activation of iNOS in response to virus infection, and consistent with the effects of BEL enantiomers on iNOS expression, (S)-BEL more effectively inhibits EMCV-induced CREB phosphorylation than (R)-BEL in macrophages. Cyclic AMP 0-4 nitric oxide synthase 2 Homo sapiens 225-229 15528042-0 2004 Dual role of cAMP in iNOS expression in glial cells and macrophages is mediated by differential regulation of p38-MAPK/ATF-2 activation and iNOS stability. Cyclic AMP 13-17 nitric oxide synthase 2 Homo sapiens 21-25 15617735-5 2005 The IC51-mediated induction of cAMP levels, downstream target of A2A and A2B, and inhibition of LPS/IFNgamma-induced expression of iNOS by forskolin, a cAMP activator, document a role for cAMP mediated pathway in anti-inflammatory activity of IC51. Cyclic AMP 152-156 nitric oxide synthase 2 Homo sapiens 131-135 15617735-5 2005 The IC51-mediated induction of cAMP levels, downstream target of A2A and A2B, and inhibition of LPS/IFNgamma-induced expression of iNOS by forskolin, a cAMP activator, document a role for cAMP mediated pathway in anti-inflammatory activity of IC51. Cyclic AMP 152-156 nitric oxide synthase 2 Homo sapiens 131-135 15617735-6 2005 Taken together, these studies document that IC51-mediated inhibition of iNOS expression is through activation of adenosine receptors, which activates A2A and A2B resulting in increased cAMP levels following LPS/IFNgamma stimulation. Cyclic AMP 185-189 nitric oxide synthase 2 Homo sapiens 72-76 15528042-5 2004 More importantly, the iNOS protein levels were equalized by the MG132 posttreatment in macrophages treated with LPS/IFN alone and along with FSK, and ubiquitinated iNOS protein levels were reduced by FSK posttreatment, suggesting that the FSK-mediated inhibition of ubiquitination of iNOS protein and the following increased stability of iNOS protein are one of the mechanisms of cAMP-pathway-mediated enhancement of iNOS gene expression in macrophages. Cyclic AMP 380-384 nitric oxide synthase 2 Homo sapiens 22-26 15528042-5 2004 More importantly, the iNOS protein levels were equalized by the MG132 posttreatment in macrophages treated with LPS/IFN alone and along with FSK, and ubiquitinated iNOS protein levels were reduced by FSK posttreatment, suggesting that the FSK-mediated inhibition of ubiquitination of iNOS protein and the following increased stability of iNOS protein are one of the mechanisms of cAMP-pathway-mediated enhancement of iNOS gene expression in macrophages. Cyclic AMP 380-384 nitric oxide synthase 2 Homo sapiens 164-168 15528042-5 2004 More importantly, the iNOS protein levels were equalized by the MG132 posttreatment in macrophages treated with LPS/IFN alone and along with FSK, and ubiquitinated iNOS protein levels were reduced by FSK posttreatment, suggesting that the FSK-mediated inhibition of ubiquitination of iNOS protein and the following increased stability of iNOS protein are one of the mechanisms of cAMP-pathway-mediated enhancement of iNOS gene expression in macrophages. Cyclic AMP 380-384 nitric oxide synthase 2 Homo sapiens 164-168 15528042-0 2004 Dual role of cAMP in iNOS expression in glial cells and macrophages is mediated by differential regulation of p38-MAPK/ATF-2 activation and iNOS stability. Cyclic AMP 13-17 nitric oxide synthase 2 Homo sapiens 140-144 15528042-5 2004 More importantly, the iNOS protein levels were equalized by the MG132 posttreatment in macrophages treated with LPS/IFN alone and along with FSK, and ubiquitinated iNOS protein levels were reduced by FSK posttreatment, suggesting that the FSK-mediated inhibition of ubiquitination of iNOS protein and the following increased stability of iNOS protein are one of the mechanisms of cAMP-pathway-mediated enhancement of iNOS gene expression in macrophages. Cyclic AMP 380-384 nitric oxide synthase 2 Homo sapiens 164-168 15528042-5 2004 More importantly, the iNOS protein levels were equalized by the MG132 posttreatment in macrophages treated with LPS/IFN alone and along with FSK, and ubiquitinated iNOS protein levels were reduced by FSK posttreatment, suggesting that the FSK-mediated inhibition of ubiquitination of iNOS protein and the following increased stability of iNOS protein are one of the mechanisms of cAMP-pathway-mediated enhancement of iNOS gene expression in macrophages. Cyclic AMP 380-384 nitric oxide synthase 2 Homo sapiens 164-168 15528042-1 2004 We reported previously that cAMP analogues or cAMP synthesis activator (forskolin; FSK) inhibit lipopolysaccharide (LPS)-induced inducible nitric-oxide systase (iNOS) gene expression in astrocytes, while they enhance that in macrophages. Cyclic AMP 28-32 nitric oxide synthase 2 Homo sapiens 129-159 15528042-6 2004 To our knowledge, this is the first evidence that cAMP regulates iNOS expression at the posttranslational level in macrophages. Cyclic AMP 50-54 nitric oxide synthase 2 Homo sapiens 65-69 15528042-1 2004 We reported previously that cAMP analogues or cAMP synthesis activator (forskolin; FSK) inhibit lipopolysaccharide (LPS)-induced inducible nitric-oxide systase (iNOS) gene expression in astrocytes, while they enhance that in macrophages. Cyclic AMP 28-32 nitric oxide synthase 2 Homo sapiens 161-165 15528042-1 2004 We reported previously that cAMP analogues or cAMP synthesis activator (forskolin; FSK) inhibit lipopolysaccharide (LPS)-induced inducible nitric-oxide systase (iNOS) gene expression in astrocytes, while they enhance that in macrophages. Cyclic AMP 46-50 nitric oxide synthase 2 Homo sapiens 129-159 15528042-1 2004 We reported previously that cAMP analogues or cAMP synthesis activator (forskolin; FSK) inhibit lipopolysaccharide (LPS)-induced inducible nitric-oxide systase (iNOS) gene expression in astrocytes, while they enhance that in macrophages. Cyclic AMP 46-50 nitric oxide synthase 2 Homo sapiens 161-165 14568676-4 2003 In particular, we demonstrate that exogenous NO inhibits PGE2 release evoked by IL-1beta whereas high levels of the prostanoid, in the presence of proinflammatory agents, exert a negative feed-back control on iNOS mRNA expression, possibly through a cAMP-dependent mechanism. Cyclic AMP 250-254 nitric oxide synthase 2 Homo sapiens 209-213 15115662-1 2004 cAMP significantly inhibits IL-1beta+IFNgamma-induced iNOS gene expression in hepatocytes, but the signaling pathways responsible for the effect are not known. Cyclic AMP 0-4 nitric oxide synthase 2 Homo sapiens 54-58 15115662-3 2004 The JNK inhibitor, SP 600125, effectively reversed the inhibitory effects of cAMP on iNOS expression and significantly increased iNOS promoter activity. Cyclic AMP 77-81 nitric oxide synthase 2 Homo sapiens 85-89 15115662-7 2004 We conclude that JNK signaling plays an important role in the inhibitory effects of cAMP on IL-1beta+IFNgamma-induced iNOS gene expression in cultured hepatocytes. Cyclic AMP 84-88 nitric oxide synthase 2 Homo sapiens 118-122 15380928-9 2004 The effects on iNOS are most likely transduced through phosphatidylinositol 3"-kinase and are counteracted by raising islet cyclic AMP levels. Cyclic AMP 124-134 nitric oxide synthase 2 Homo sapiens 15-19 12895436-4 2003 Both the inhibitory and stimulatory effects of cAMP on adenovirus mediated iNOS expression were dose dependent. Cyclic AMP 47-51 nitric oxide synthase 2 Homo sapiens 75-79 12895436-5 2003 This dual effect of cAMP on iNOS activity and expression can be accounted by its effect on CMV promoter activity since dbcAMP significantly inhibited CMV promoter activity in hepatocytes at low concentration and induced it at high concentration. Cyclic AMP 20-24 nitric oxide synthase 2 Homo sapiens 28-32 14561177-0 2003 Regulation of inducible nitric oxide synthase by cAMP-elevating phospho-diesterase inhibitors. Cyclic AMP 49-53 nitric oxide synthase 2 Homo sapiens 14-45 14561177-1 2003 Among the numerous genes controlled by cyclic adenosine monophosphate (cAMP)/protein kinase A signalling machinery is the gene encoding the inducible nitric oxide synthase (iNOS), an enzyme catalyzing the synthesis of a highly reactive free radical nitric oxide (NO). Cyclic AMP 71-75 nitric oxide synthase 2 Homo sapiens 173-177 14561177-3 2003 A feasible way for cAMP-dependent therapeutic control of inflammation, including iNOS-mediated NO synthesis, could involve the administration of drugs that block the enzymatic activity of cAMP-degrading phosphodiesterases (PDE). Cyclic AMP 19-23 nitric oxide synthase 2 Homo sapiens 81-85 14561177-3 2003 A feasible way for cAMP-dependent therapeutic control of inflammation, including iNOS-mediated NO synthesis, could involve the administration of drugs that block the enzymatic activity of cAMP-degrading phosphodiesterases (PDE). Cyclic AMP 188-192 nitric oxide synthase 2 Homo sapiens 81-85 14561177-1 2003 Among the numerous genes controlled by cyclic adenosine monophosphate (cAMP)/protein kinase A signalling machinery is the gene encoding the inducible nitric oxide synthase (iNOS), an enzyme catalyzing the synthesis of a highly reactive free radical nitric oxide (NO). Cyclic AMP 39-69 nitric oxide synthase 2 Homo sapiens 140-171 14561177-4 2003 Indeed, cAMP-elevating PDE inhibitors can influence iNOS activation in different cell types in vitro, and their potent anti-inflammatory effects in experimental disease models and clinical studies were frequently accompanied with profound modulation of NO production. Cyclic AMP 8-12 nitric oxide synthase 2 Homo sapiens 52-56 14561177-5 2003 A set of conflicting data has been generated over the years, ranging from strong suppression to marked enhancement of NO release by cAMP-increasing PDE inhibitors, depending on cell-type, iNOS stimuli, and/or the agents used. Cyclic AMP 132-136 nitric oxide synthase 2 Homo sapiens 188-192 14561177-6 2003 The present review summarizes the data on iNOS modulation by cAMP-elevating PDE inhibitors and possible mechanisms behind it, speculating on its contribution to the therapeutic effects of these drugs. Cyclic AMP 61-65 nitric oxide synthase 2 Homo sapiens 42-46 14561177-1 2003 Among the numerous genes controlled by cyclic adenosine monophosphate (cAMP)/protein kinase A signalling machinery is the gene encoding the inducible nitric oxide synthase (iNOS), an enzyme catalyzing the synthesis of a highly reactive free radical nitric oxide (NO). Cyclic AMP 39-69 nitric oxide synthase 2 Homo sapiens 173-177 14561177-1 2003 Among the numerous genes controlled by cyclic adenosine monophosphate (cAMP)/protein kinase A signalling machinery is the gene encoding the inducible nitric oxide synthase (iNOS), an enzyme catalyzing the synthesis of a highly reactive free radical nitric oxide (NO). Cyclic AMP 71-75 nitric oxide synthase 2 Homo sapiens 140-171 12119468-9 2002 CONCLUSIONS: An IP receptor mediated increase in cyclic adenosine monophosphate formation plays an important role in enhancing LPS/IFN-gamma-induced iNOS expression in human monocytes/macrophages and may, therefore, contribute to the increased production of NO during peritonitis. Cyclic AMP 49-79 nitric oxide synthase 2 Homo sapiens 149-153 12458038-2 2002 Inducible NOS expression is regulated by intracellular adenosine 3",5"-cyclic monophosphate (cAMP) signaling, and astrocytes contain both iNOS and adenylate cyclase-coupled neurotransmitter receptors. Cyclic AMP 55-91 nitric oxide synthase 2 Homo sapiens 0-13 12458038-2 2002 Inducible NOS expression is regulated by intracellular adenosine 3",5"-cyclic monophosphate (cAMP) signaling, and astrocytes contain both iNOS and adenylate cyclase-coupled neurotransmitter receptors. Cyclic AMP 93-97 nitric oxide synthase 2 Homo sapiens 0-13 12458038-9 2002 In conclusion, it appears that DA attenuates iNOS through a D(1), beta1 and beta2 adrenergic receptor-linked adenylate cyclase-mediated cAMP cascade. Cyclic AMP 136-140 nitric oxide synthase 2 Homo sapiens 45-49 10593859-0 1999 Regulation of the expression of the inflammatory nitric oxide synthase (NOS2) by cyclic AMP. Cyclic AMP 81-91 nitric oxide synthase 2 Homo sapiens 72-76 11827727-5 2000 These results suggest that enhancing effects of PTX on the iNOS gene expression in the IL-1beta-stimulated VSMCs is mediated predominantly through the activation of NF-kappaB via cAMP-dependent PKA pathway. Cyclic AMP 179-183 nitric oxide synthase 2 Homo sapiens 59-63 10779013-1 2000 The authors studied whether cyclic AMP (cAMP), a widespread regulator of inflammation, modulates the cytokine-mediated expression of the intercellular adhesion molecule, intercellular adhesion molecule-1 (ICAM-1), and the inflammatory nitric oxide synthase 2 (NOS-2), in primary and immortalized brain endothelial cell cultures (GP8.3 cell line). Cyclic AMP 28-38 nitric oxide synthase 2 Homo sapiens 235-258 10779013-1 2000 The authors studied whether cyclic AMP (cAMP), a widespread regulator of inflammation, modulates the cytokine-mediated expression of the intercellular adhesion molecule, intercellular adhesion molecule-1 (ICAM-1), and the inflammatory nitric oxide synthase 2 (NOS-2), in primary and immortalized brain endothelial cell cultures (GP8.3 cell line). Cyclic AMP 28-38 nitric oxide synthase 2 Homo sapiens 260-265 10593859-4 1999 Since cyclic AMP inhibits numerous immunological reactions, studies have been carried out to determine whether cAMP-dependent pathways could inhibit NOS2 expression as well. Cyclic AMP 111-115 nitric oxide synthase 2 Homo sapiens 149-153 10593859-5 1999 Pharmacological studies in cultured cells show that, depending on the cell type examined, increased cAMP can exert opposite effects on the endotoxin- or cytokine-induced expression of NOS2, being either stimulatory or inhibitory in macrophages, stimulatory in adipocytes, smooth muscle, skeletal muscle, and brain endothelial cells, and inhibitory in pancreatic, liver, and brain glial cells. Cyclic AMP 100-104 nitric oxide synthase 2 Homo sapiens 184-188 10593859-6 1999 Regulation of NOS2 gene transcription appears to be the primary mechanism of action of cAMP, and whether it is stimulatory or inhibitory hinges on the cell-specific regulation of transcription factors including CREB, NF-kappaB, and C/EBP. Cyclic AMP 87-91 nitric oxide synthase 2 Homo sapiens 14-18 10593859-8 1999 This review summarizes evidence derived from in vitro studies, considers regulation of NOS2 by cAMP in vivo, and discusses possible therapeutic applications of cAMP treatment.-Galea, E., Feinstein, D. L. Regulation of the expression of the inflammatory nitric oxide synthase (NOS2) by cyclic AMP. Cyclic AMP 95-99 nitric oxide synthase 2 Homo sapiens 87-91 9588181-0 1998 Inducible nitric oxide synthase (iNOS) expression in human monocytes triggered by beta-endorphin through an increase in cAMP. Cyclic AMP 120-124 nitric oxide synthase 2 Homo sapiens 0-31 10531359-9 1999 The direct PKA activator, Bt(2)cAMP, caused concentration-dependent NO release and iNOS expression, as confirmed by immunofluorescence studies. Cyclic AMP 31-35 nitric oxide synthase 2 Homo sapiens 83-87 10531359-11 1999 Two cAMP-elevating agents, forskolin and cholera toxin, potentiated the LPS-induced NO release and iNOS expression. Cyclic AMP 4-8 nitric oxide synthase 2 Homo sapiens 99-103 10531359-15 1999 These results suggest that 6 h of treatment with LPS increases intracellular cAMP levels via COX-2 induction and prostaglandin E(2) production, resulting in PKA activation, NF-kappaB activation, iNOS expression, and NO production. Cyclic AMP 77-81 nitric oxide synthase 2 Homo sapiens 195-199 9641464-12 1998 These data suggest that cAMP is required for the induction of iNOS in ECs and that NO may directly impair adenylate cyclase activity, preventing iNOS activation. Cyclic AMP 24-28 nitric oxide synthase 2 Homo sapiens 62-66 10446104-0 1999 Potentiation of cytokine induced iNOS expression in the human intestinal epithelial cell line, DLD-1, by cyclic AMP. Cyclic AMP 105-115 nitric oxide synthase 2 Homo sapiens 33-37 10446104-2 1999 AIMS: To examine the effects of cAMP, an intracellular mediator of several proinflammatory mediators, on iNOS expression in the human intestinal epithelial cell line, DLD-1. Cyclic AMP 32-36 nitric oxide synthase 2 Homo sapiens 105-109 10446104-9 1999 The cAMP analogues potentiated iNOS at the transcriptional level as shown by effects of actinomycin D (5 microgram/ml) and northern blot analyses; the nuclear factor (NF) kappaB inhibitor, pyrrolidine dithiocarbamate (10-200 microM), significantly reduced this potentiation. Cyclic AMP 4-8 nitric oxide synthase 2 Homo sapiens 31-35 10446104-10 1999 The cAMP potentiated iNOS activity was inhibited by the tyrosine kinase inhibitor, A25 (10-200 microM) and the Janus activated kinase 2 inhibitor, B42 (10-200 microM). Cyclic AMP 4-8 nitric oxide synthase 2 Homo sapiens 21-25 10446104-11 1999 CONCLUSIONS: Increased intracellular cAMP is a potent stimulus of iNOS expression in combination with cytokines in DLD-1 cells, acting at the transcriptional level and involving NF-kappaB and the JAK-STAT pathways. Cyclic AMP 37-41 nitric oxide synthase 2 Homo sapiens 66-70 10446104-12 1999 Thus, proinflammatory mediators that increase cAMP levels may augment iNOS expression and NO production. Cyclic AMP 46-50 nitric oxide synthase 2 Homo sapiens 70-74 10440125-0 1999 Human vascular smooth muscle cells express a constitutive nitric oxide synthase that insulin rapidly activates, thus increasing guanosine 3":5"-cyclic monophosphate and adenosine 3":5"-cyclic monophosphate concentrations. Cyclic AMP 169-205 nitric oxide synthase 2 Homo sapiens 58-79 9588181-0 1998 Inducible nitric oxide synthase (iNOS) expression in human monocytes triggered by beta-endorphin through an increase in cAMP. Cyclic AMP 120-124 nitric oxide synthase 2 Homo sapiens 33-37 9588181-4 1998 The possible relationship between cAMP and iNOS expression on monocytes was investigated. Cyclic AMP 34-38 nitric oxide synthase 2 Homo sapiens 43-47 9588181-6 1998 The cAMP level raised by beta-endorphin was lowered by naloxone, which also reduced slightly iNOS expression. Cyclic AMP 4-8 nitric oxide synthase 2 Homo sapiens 93-97 9374723-11 1997 Speculatively, if the LPS-independent iNOS pathway exists in humans, the iNOS in tissues from patients taking drugs affecting cAMP or P2y receptors may be iatrogenic rather than pathogenetic in origin. Cyclic AMP 126-130 nitric oxide synthase 2 Homo sapiens 73-77 9294835-2 1997 Because acetate induces production of cAMP, which is a powerful stimulus of NO synthase (NOS), we evaluated the effect of different dialysate solutions with and without acetate on NOS activity in endothelial cells (EC). Cyclic AMP 38-42 nitric oxide synthase 2 Homo sapiens 76-87 8858119-8 1996 It is possible that the increase in iNOS found in asthmatic patients and those with other diseases that are treated with drugs which affect the cAMP and purine systems may be iatrogenic rather than pathogenetic in origin. Cyclic AMP 144-148 nitric oxide synthase 2 Homo sapiens 36-40 9301524-0 1997 Differential regulation of IFN-gamma, IL-10 and inducible nitric oxide synthase in human T cells by cyclic AMP-dependent signal transduction pathway. Cyclic AMP 100-110 nitric oxide synthase 2 Homo sapiens 48-79 8904645-3 1996 In addition the interaction between cyclic AMP- and cyclic GMP-elevating agonists on the IL-1 beta-stimulated expression of iNOS was examined. Cyclic AMP 36-46 nitric oxide synthase 2 Homo sapiens 124-128 7521256-12 1994 These data demonstrate a major effect of cyclic AMP on cytokine-induced NOS activity in VSM cells, mediated at least in part by regulating synthesis of iNOS, and has implications for the pathogenesis and management of septic shock. Cyclic AMP 41-51 nitric oxide synthase 2 Homo sapiens 152-156 8601429-8 1996 They also suggest that reactive oxygen intermediates do not play a role in the activation of NF-kappa B by IL-1 beta in VSMC, and that transcription factors other than NF-kappa B mediate the induction of iNOS expression by elevating the intracellular concentration of cyclic AMP. Cyclic AMP 268-278 nitric oxide synthase 2 Homo sapiens 204-208 33000885-5 2020 First, cAMP-induced PP2Ac nitration was significantly repressed using L-NAME, an inhibitor of nitric oxide synthase (NOS). Cyclic AMP 7-11 nitric oxide synthase 2 Homo sapiens 94-115 7693710-4 1993 Forskolin, a direct activator of adenylate cyclase, or dibutyryl cAMP alone caused small increases in nitrite accumulation and iNOS mRNA and protein levels and synergistically enhanced the IFN-gamma-stimulated reactions. Cyclic AMP 65-69 nitric oxide synthase 2 Homo sapiens 127-131 7693710-8 1993 These results indicate that an elevation of intracellular cAMP, particularly in combination with inflammatory cytokines, positively regulates nitric oxide production at the level of iNOS mRNA expression in vascular smooth muscle cells. Cyclic AMP 58-62 nitric oxide synthase 2 Homo sapiens 182-186 33000885-7 2020 Second, cAMP-induced iNOS expression and PP2Ac nitration were decreased by treatment with TSA, an inhibitor of histone deacetylase 5 (HDAC5). Cyclic AMP 8-12 nitric oxide synthase 2 Homo sapiens 21-25 25125801-6 2014 Moreover, CCK restored the intracellular cAMP content activating the protein kinase A (PKA) pathway, which resulted in a negative modulatory role on iNOS expression. Cyclic AMP 41-45 nitric oxide synthase 2 Homo sapiens 149-153 24291824-8 2013 Thus, cAMP has a dual effect on immune reactions; cAMP up-regulated IL-6 expression, but down-regulated iNOS expression under ER stress. Cyclic AMP 6-10 nitric oxide synthase 2 Homo sapiens 104-108 24291824-8 2013 Thus, cAMP has a dual effect on immune reactions; cAMP up-regulated IL-6 expression, but down-regulated iNOS expression under ER stress. Cyclic AMP 50-54 nitric oxide synthase 2 Homo sapiens 104-108 20934465-4 2011 We hypothesized that Akt mediates the effect of cAMP on hepatocyte iNOS expression. Cyclic AMP 48-52 nitric oxide synthase 2 Homo sapiens 67-71 23143065-2 2013 Cyclic adenosine monophosphate inhibits cytokine-induced expression of inducible nitric oxide synthase (iNOS) in hepatocytes by a protein kinase A-independent mechanism. Cyclic AMP 0-30 nitric oxide synthase 2 Homo sapiens 71-102 23143065-2 2013 Cyclic adenosine monophosphate inhibits cytokine-induced expression of inducible nitric oxide synthase (iNOS) in hepatocytes by a protein kinase A-independent mechanism. Cyclic AMP 0-30 nitric oxide synthase 2 Homo sapiens 104-108 23143065-4 2013 A cyclic AMP analog that specifically activates Epac, 8-(4-methoxyphenylthio)-2"-O-methyladenosine-3",5"-cyclic monophosphate (OPTmecAMP), and overexpression of liver-specific Epac2 both inhibited interleukin 1beta/interferon gamma-induced iNOS expression and nitrite production. Cyclic AMP 2-12 nitric oxide synthase 2 Homo sapiens 240-244 22687049-12 2012 CONCLUSION: Our results suggest that in islets from type 2 diabetes, stimulatory effects in certain cAMP-compartments induced by PDE inhibitors might play a central role in the suppression of iNOS, resulting in increased beta-cell viability and improved secretory response to glucose. Cyclic AMP 100-104 nitric oxide synthase 2 Homo sapiens 192-196 20934465-7 2011 The cyclic AMP-induced suppression of cytokine-stimulated iNOS was partially reversed by LY294002 and FTI-276. Cyclic AMP 4-14 nitric oxide synthase 2 Homo sapiens 58-62