PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12393539-3 2003 Here, using primary human T lymphocytes in which endogenous cAMP was increased by the use of forskolin and 3-isobutyl-1-methylxanthine (IBMX), we show that increase of cAMP resulted in inhibition of T-cell receptor (TCR)/CD3 plus CD28-mediated T-cell activation and cytokine production and blockade of cell cycle progression at the G(1) phase. Colforsin 93-102 cathelicidin antimicrobial peptide Homo sapiens 60-64 12421748-4 2003 Taurochenodeoxycholate and tauroursodeoxycholate increased forskolin-induced cAMP accumulation to a similar extent, without affecting cAMP basal levels. Colforsin 59-68 cathelicidin antimicrobial peptide Homo sapiens 77-81 12393539-3 2003 Here, using primary human T lymphocytes in which endogenous cAMP was increased by the use of forskolin and 3-isobutyl-1-methylxanthine (IBMX), we show that increase of cAMP resulted in inhibition of T-cell receptor (TCR)/CD3 plus CD28-mediated T-cell activation and cytokine production and blockade of cell cycle progression at the G(1) phase. Colforsin 93-102 cathelicidin antimicrobial peptide Homo sapiens 168-172 12053213-6 2002 Forskolin and 8-Br-cyclic adenosine monophosphate (cAMP) were used to activate cAMP-dependent Cl? Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 79-83 12053213-11 2002 In contrast, long-term exposure (24 hours) to physiological concentrations of progesterone (100 nM), but not estradiol, dose-dependently reduced the peak Isc induced by the cAMP-agonist forskolin from 125 +/- 2.7 mA. Colforsin 186-195 cathelicidin antimicrobial peptide Homo sapiens 173-177 11548900-8 2001 Addition of cAMP (10(-10) to 10(-5) M) caused a significant (P < 0.01) increase in CBF, whereas depletion of endogenous cAMP after pre-incubation with the adenylate cyclase activator forskolin (10(-5) M) prevented the PGE2-induced increase in CBF (P > 0.05). Colforsin 186-195 cathelicidin antimicrobial peptide Homo sapiens 12-16 11469886-9 2001 Conversely, cAMP enhanced LPS-stimulated IL-10 release (100 +/- 21.5 pg/10(6) cells in LPS + dbcAMP and 110 +/- 25.2 pg/10(6) cells in LPS + FSK, both P < 0.05 vs 53.3 +/- 12.8 pg/10(6) cells in LPS alone). Colforsin 141-144 cathelicidin antimicrobial peptide Homo sapiens 12-16 11469886-8 2001 RESULTS: cAMP-elevating agents inhibited LPS-stimulated TNF-alpha release (0.77 +/- 0.13 ng/10(6) cells in LPS + dbcAMP and 0.68 +/- 0.19 ng/10(6) cells in LPS + FSK, both P < 0.05 vs 1.61 +/- 0.34 ng/10(6) cells in LPS alone). Colforsin 162-165 cathelicidin antimicrobial peptide Homo sapiens 9-13 11548900-8 2001 Addition of cAMP (10(-10) to 10(-5) M) caused a significant (P < 0.01) increase in CBF, whereas depletion of endogenous cAMP after pre-incubation with the adenylate cyclase activator forskolin (10(-5) M) prevented the PGE2-induced increase in CBF (P > 0.05). Colforsin 186-195 cathelicidin antimicrobial peptide Homo sapiens 123-127 10777606-3 2000 Furthermore, forskolin, which increases intracellular cAMP levels, also effectively suppressed TNFalpha+ActD-induced apoptosis. Colforsin 13-22 cathelicidin antimicrobial peptide Homo sapiens 54-58 11516507-7 2001 Activity was evaluated by measurements of the inhibition of forskolin-stimulated 3",5"-cyclic adenosine monophosphate (c-AMP) performing competitive binding assays. Colforsin 60-69 cathelicidin antimicrobial peptide Homo sapiens 119-124 10843764-6 2000 IFN-gamma also synergistically augmented HGF production induced by interleukin-1beta and cAMP-increasing agents cholera toxin, forskolin and prostaglandin E(2). Colforsin 127-136 cathelicidin antimicrobial peptide Homo sapiens 89-93 10856433-7 2000 In contrast, PDE4 inhibitors increased the forskolin-induced cellular cAMP concentration 13- to 17-fold above control. Colforsin 43-52 cathelicidin antimicrobial peptide Homo sapiens 70-74 9515168-4 1998 Phagocytosis and accumulation of PDE-4 and PKA near adherent zymosan were inhibited by elevating cAMP levels with forskolin or rolipram. Colforsin 114-123 cathelicidin antimicrobial peptide Homo sapiens 97-101 10779013-4 2000 Stimulation of cAMP-dependent pathways with forskolin or dibutyryl cAMP decreased ICAM-1 protein expression, whereas it increased NOS-2 protein expression. Colforsin 44-53 cathelicidin antimicrobial peptide Homo sapiens 15-19 9793684-9 1998 Furthermore, direct activation of the cellular adenylyl cyclase activity by treatment with forskolin alone induced a prompt Ca2+ signal in the presence, but not in the absence, of extracellular Ca2+, identical results were obtained with the cell permeable cAMP analogue 8-bromo-cAMP. Colforsin 91-100 cathelicidin antimicrobial peptide Homo sapiens 256-260 9793684-9 1998 Furthermore, direct activation of the cellular adenylyl cyclase activity by treatment with forskolin alone induced a prompt Ca2+ signal in the presence, but not in the absence, of extracellular Ca2+, identical results were obtained with the cell permeable cAMP analogue 8-bromo-cAMP. Colforsin 91-100 cathelicidin antimicrobial peptide Homo sapiens 278-282 9721879-11 1998 In these, forskolin (with or without Dex) caused a similar increase in cAMP (approximately 300-fold) and phospho-cAMP-responsive element binding protein (approximately 4-5-fold) levels, whereas total cAMP-responsive element binding protein expression was not affected. Colforsin 10-19 cathelicidin antimicrobial peptide Homo sapiens 71-75 9721879-11 1998 In these, forskolin (with or without Dex) caused a similar increase in cAMP (approximately 300-fold) and phospho-cAMP-responsive element binding protein (approximately 4-5-fold) levels, whereas total cAMP-responsive element binding protein expression was not affected. Colforsin 10-19 cathelicidin antimicrobial peptide Homo sapiens 113-117 9721879-11 1998 In these, forskolin (with or without Dex) caused a similar increase in cAMP (approximately 300-fold) and phospho-cAMP-responsive element binding protein (approximately 4-5-fold) levels, whereas total cAMP-responsive element binding protein expression was not affected. Colforsin 10-19 cathelicidin antimicrobial peptide Homo sapiens 113-117 9507195-2 1998 Multifibre nerve responses during noxious heating were enhanced by adding forskolin, an agent that elevates cAMP. Colforsin 74-83 cathelicidin antimicrobial peptide Homo sapiens 108-112 1310554-12 1992 Promoter function of both FIV LTRs was also enhanced in cells treated with either forskolin, an inducer of intracellular cyclic-AMP (c-AMP), or dibutyryl c-AMP. Colforsin 82-91 cathelicidin antimicrobial peptide Homo sapiens 126-131 8944640-2 1996 In CFPAC-1 cells, adenosine 3",5"-cyclic monophosphate (cAMP) stimulation with forskolin (10 microM) plus 8-(4-chlorophenylthio)adenosine 3",5"-cyclic monophosphate (400 microM) activated neither Cl- nor K+ currents. Colforsin 79-88 cathelicidin antimicrobial peptide Homo sapiens 56-60 8836034-8 1996 The segment of the D1A gene between these two cAMP-responsive regions contained two additional DNA-protein interaction sites, one of which bound to nuclear factors considerably stronger following forskolin/IBMX treatment. Colforsin 196-205 cathelicidin antimicrobial peptide Homo sapiens 46-50 1328629-8 1992 A significant increase in the cAMP content in the follicle was observed within 30 min, but the ability to produce cAMP in response to forskolin decreased as the duration of perfusion was increased. Colforsin 134-143 cathelicidin antimicrobial peptide Homo sapiens 114-118 1328629-9 1992 Intraoocyte cAMP increased significantly within 30 min and reached its maximum 2 h after exposure to forskolin. Colforsin 101-110 cathelicidin antimicrobial peptide Homo sapiens 12-16 1328629-12 1992 The alterations of intraoocyte cAMP contents following exposure to hCG in vivo paralleled those observed in the ovaries perfused with forskolin. Colforsin 134-143 cathelicidin antimicrobial peptide Homo sapiens 31-35 1378435-8 1992 Furthermore, elevation of cAMP, either through receptor-mediated mechanisms (e.g. prostaglandin E1) or by direct stimulation of adenylate cyclase (e.g. forskolin), also caused a marked dose-dependent depletion of 80K/MARCKS mRNA levels, which were further reduced by co-administration with cAMP-phosphodiesterase inhibitors. Colforsin 152-161 cathelicidin antimicrobial peptide Homo sapiens 26-30 1378435-8 1992 Furthermore, elevation of cAMP, either through receptor-mediated mechanisms (e.g. prostaglandin E1) or by direct stimulation of adenylate cyclase (e.g. forskolin), also caused a marked dose-dependent depletion of 80K/MARCKS mRNA levels, which were further reduced by co-administration with cAMP-phosphodiesterase inhibitors. Colforsin 152-161 cathelicidin antimicrobial peptide Homo sapiens 290-294 9546582-9 1998 Cyclic AMP derivatives or cAMP generating agents such as PTH and forskolin inhibited ERK2 activation by bFGF and PDGF-BB suggesting a "cross-talk" between the two different signalling pathways activated by receptor tyrosine kinases and cAMP-dependent protein kinase. Colforsin 65-74 cathelicidin antimicrobial peptide Homo sapiens 26-30 9546582-9 1998 Cyclic AMP derivatives or cAMP generating agents such as PTH and forskolin inhibited ERK2 activation by bFGF and PDGF-BB suggesting a "cross-talk" between the two different signalling pathways activated by receptor tyrosine kinases and cAMP-dependent protein kinase. Colforsin 65-74 cathelicidin antimicrobial peptide Homo sapiens 236-240 8554613-1 1995 Neutrophil apoptosis, determined after 20 h in culture using standard criteria and shedding of cell surface CD16 (Fc gamma RIII), is dramatically inhibited, in a concentration-dependent manner, by the cAMP analogs, dibutyryl-cAMP and 8-Br-cAMP, and the adenylyl cyclase activator, forskolin. Colforsin 281-290 cathelicidin antimicrobial peptide Homo sapiens 201-205 7785987-8 1995 Forskolin, rolipram, and dibutyryl-cAMP, which are known to increase intracellular cAMP levels, also shortened neutrophil survival. Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 83-87 7995950-5 1995 FMLP-mediated adhesion was inhibited by a diverse group of cAMP modulators: forskolin, isoproterenol, phosphodiesterase IV inhibitors (rolipram and Ro 20-1724), but not phosphodiesterase III inhibitors (milrinone and bemoradan). Colforsin 76-85 cathelicidin antimicrobial peptide Homo sapiens 59-63 7786447-6 1994 Forskolin and vanadate significantly increased cellular cAMP level, while carbachol and AlF4- did not. Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 56-60 8384558-6 1993 In mature CTL (but not in their immature precursors), T cell receptor triggering by specific targets results in a measurable increase in cAMP levels and strongly synergizes with adenylyl cyclase activators such as prostaglandin E2, cholera toxin and forskolin. Colforsin 250-259 cathelicidin antimicrobial peptide Homo sapiens 137-141 1310554-12 1992 Promoter function of both FIV LTRs was also enhanced in cells treated with either forskolin, an inducer of intracellular cyclic-AMP (c-AMP), or dibutyryl c-AMP. Colforsin 82-91 cathelicidin antimicrobial peptide Homo sapiens 133-138 2467944-3 1989 This induction is most likely due to the increase in cAMP levels elicited by the agonist, based on the direct measurements of cAMP levels and the ability of DBcAMP and the adenylate cyclase activator, forskolin to mimic the effects of isoproterenol. Colforsin 201-210 cathelicidin antimicrobial peptide Homo sapiens 53-57 1745821-15 1991 By contrast, cAMP induces in essence gene activation in WI26VA4 transformed human lung fibroblasts in which renin mRNA levels increase by up to 150-fold in response to forskolin. Colforsin 168-177 cathelicidin antimicrobial peptide Homo sapiens 13-17 2175792-4 1990 This pattern of protein phosphorylation is identical to that observed when the platelets were treated with forskolin, phosphodiesterase inhibitors or other compounds that elevate platelet cAMP levels. Colforsin 107-116 cathelicidin antimicrobial peptide Homo sapiens 188-192 2177182-2 1990 In the present study, forskolin and histamine [agonists that increase intracellular cyclic adenosine monophosphate (cAMP)], and dibutyryl cAMP, activated channels in previously quiescent cell-attached membrane patches on cultured human gastric cells (HGT-1). Colforsin 22-31 cathelicidin antimicrobial peptide Homo sapiens 116-120 34166397-5 2021 Forskolin alone and with IL-1beta increased IkappaBalpha mRNA expression suggesting that in the context of inflammation and in the presence of AKIP1, cAMP enhances p65 activation. Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 150-154 2166109-3 1990 The exposure of murine or human T cells to dibutyryl cAMP or the cAMP-elevating drug, forskolin, resulted in a decrease in high affinity IL-2 binding. Colforsin 86-95 cathelicidin antimicrobial peptide Homo sapiens 65-69 9795233-3 1998 In [32P]i-prelabeled platelets, forskolin increased intracellular cAMP (104 nmol/1011 cells at 10-5 M forskolin) and [32P]phosphatidylinositol 4-phosphate (Delta[32P]PIP) (30% at 10-7-10-6 M forskolin). Colforsin 32-41 cathelicidin antimicrobial peptide Homo sapiens 66-70 9795233-9 1998 The inverse relation between forskolin-produced DeltaPIP and [32P]PA production suggests that the PLC reaction is inhibited by elevated cAMP through reduction of substrate (PIP2) resynthesis, and not by inhibition of the PLC enzyme. Colforsin 29-38 cathelicidin antimicrobial peptide Homo sapiens 136-140 34166397-2 2021 Here, we have extended these observations, using primary myometrial cell cultures to show that the cAMP agonist, forskolin, enhances IL-1beta-driven COX-2 expression. Colforsin 113-122 cathelicidin antimicrobial peptide Homo sapiens 99-103 2457366-3 1988 It was observable regardless of whether basal, PGE1- or forskolin-stimulated cAMP levels were measured. Colforsin 56-65 cathelicidin antimicrobial peptide Homo sapiens 77-81 2845720-1 1987 The present experiments were designed to evaluate the effectiveness of forskolin on cAMP production, growth and morphology on cell cultures of glia, endothelium and smooth muscle derived from brain microvessels. Colforsin 71-80 cathelicidin antimicrobial peptide Homo sapiens 84-88 2835450-4 1988 The cAMP-elevating agents forskolin (5 x 10(-6)-10(-4) M) and dibutyryl cAMP (dbcAMP; 5 x 10(-3)-10(-2) M) suppressed neurite elongation and growth cone movements in identified neurons B19 (5-HT sensitive) and B5 (5-HT insensitive); the suppression was reversible. Colforsin 26-35 cathelicidin antimicrobial peptide Homo sapiens 4-8 2448308-5 1988 Other agents that raise the intracellular level of cAMP, including forskolin and isobutylmethylxanthine (IBMX) also inhibit TcR-triggered CTL activation. Colforsin 67-76 cathelicidin antimicrobial peptide Homo sapiens 51-55 2448308-7 1988 Forskolin and IBMX inhibited TcR-triggered phosphoinositide turnover in CTL, suggesting that cAMP affected very early events in signal transduction that follow TcR cross-linking by a ligand. Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 93-97 2845720-2 1987 Forskolin significantly increased formation of cAMP and decreased incorporation of thymidine in all three cell types. Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 47-51 3019646-6 1986 Treatment of small luteal cells with oLH, cholera toxin, and forskolin resulted in dose-dependent increases in cAMP in both the cells and the incubation media and in the progesterone content of the media. Colforsin 61-70 cathelicidin antimicrobial peptide Homo sapiens 111-115 2410732-9 1985 Discrepancies between cAMP formation and lipolysis during isoprenaline or forskolin stimulation have been observed, and could indicate either compartmentalization of cAMP or alternatively disprove the cAMP hypothesis. Colforsin 74-83 cathelicidin antimicrobial peptide Homo sapiens 22-26 3015387-3 1986 Desensitization is receptor mediated as indicated by: (a) the pharmacological specificity of the desensitization (VIP greater than secretin); (b) the considerable decrease of the potentiative action of VIP on forskolin-induced cAMP generation; and (c) the close temporal relationship between VIP receptor desensitization and the disappearance of the VIP binding sites from the cell surface. Colforsin 209-218 cathelicidin antimicrobial peptide Homo sapiens 227-231 3016246-9 1986 A 6-fold increase in cAMP levels was sufficient to maximally increase lipolysis with isoproterenol, whereas the maximum lipolytic response to forskolin was associated with a 20-fold increase in cAMP levels. Colforsin 142-151 cathelicidin antimicrobial peptide Homo sapiens 194-198 3016246-12 1986 At any given concentration of cAMP the corresponding lipolytic response was greater for isoproterenol than for forskolin. Colforsin 111-120 cathelicidin antimicrobial peptide Homo sapiens 30-34 3017869-2 1986 injection (experimental metastases) correlates positively with their capacity to respond to activators of cyclic adenosine 3-, 5-monophosphate (cAMP) metabolism (such as melanocyte-stimulating hormone and forskolin). Colforsin 205-214 cathelicidin antimicrobial peptide Homo sapiens 106-142 3016246-7 1986 The maximum response to isoproterenol in the presence of either theophylline or adenosine deaminase (and to forskolin) was limited by some step in the lipolytic process distal to cAMP accumulation. Colforsin 108-117 cathelicidin antimicrobial peptide Homo sapiens 179-183 3016246-8 1986 The relationships between cAMP levels and lipolysis for isoproterenol and forskolin were found to be different. Colforsin 74-83 cathelicidin antimicrobial peptide Homo sapiens 26-30 30322210-3 2018 Here, we tested the impact of cAMP/PKA (protein kinase A) signaling induced by 3-isobutyl-1 methyl xanthine (IBMX), forskolin, and 8-CPT-cAMP on the expression of Dlx5 in 3T3-L1 preadipocytes. Colforsin 116-125 cathelicidin antimicrobial peptide Homo sapiens 30-34 32949251-9 2021 The maximal cAMP response to forskolin (10 muM) was preserved in all groups. Colforsin 29-38 cathelicidin antimicrobial peptide Homo sapiens 12-16 27673556-8 2016 In vitro exposure of myometrial cells to stretch and IL-1beta increased OTR levels and reduced basal and forskolin-stimulated cAMP and PKA activity, as judged by phospho-cAMP response element-binding protein levels, but neither stretch nor IL-1beta had any effect on PKA or EPAC1 levels. Colforsin 105-114 cathelicidin antimicrobial peptide Homo sapiens 126-130 27673556-8 2016 In vitro exposure of myometrial cells to stretch and IL-1beta increased OTR levels and reduced basal and forskolin-stimulated cAMP and PKA activity, as judged by phospho-cAMP response element-binding protein levels, but neither stretch nor IL-1beta had any effect on PKA or EPAC1 levels. Colforsin 105-114 cathelicidin antimicrobial peptide Homo sapiens 170-174 22001259-7 2012 The ROCE was inhibited by forskolin and papaverine to activate the cAMP/PKA pathway, whereas it was potentiated by Rp-8-bromoadenosine-cAMP sodium salt, a PKA inhibitor. Colforsin 26-35 cathelicidin antimicrobial peptide Homo sapiens 67-71 26049102-5 2015 Incubation with forskolin, an activator of adenylyl cyclase, confirmed the association between intracellular cAMP and upregulation of MRP2. Colforsin 16-25 cathelicidin antimicrobial peptide Homo sapiens 109-113 22759971-11 2012 cAMP elevation by a physiologic agonist, isoproterenol, mimicked the results obtained with forskolin or 8-pCPT-2"-O-Me-cAMP. Colforsin 91-100 cathelicidin antimicrobial peptide Homo sapiens 0-4 26574187-5 2016 We found that acute exposure to hypercapnia significantly reduced forskolin-stimulated elevations in intracellular cAMP as well as both adenosine- and forskolin-stimulated increases in CFTR-dependent transepithelial short-circuit current, in polarised cultures of Calu-3 human airway cells. Colforsin 66-75 cathelicidin antimicrobial peptide Homo sapiens 115-119 24657252-5 2014 After treatment of cells with exogenous cAMP, forskolin (an activator of cAMP) or KH-7 (an inhibitor of cAMP), respectively, it was confirmed that cAMP communication from bystander cells to targeted cells could mitigate radiation damage in U739 cells, and this cAMP insufficiency in the bystander cells contributed to the enhancement of bystander apoptosis. Colforsin 46-55 cathelicidin antimicrobial peptide Homo sapiens 73-77 24657252-5 2014 After treatment of cells with exogenous cAMP, forskolin (an activator of cAMP) or KH-7 (an inhibitor of cAMP), respectively, it was confirmed that cAMP communication from bystander cells to targeted cells could mitigate radiation damage in U739 cells, and this cAMP insufficiency in the bystander cells contributed to the enhancement of bystander apoptosis. Colforsin 46-55 cathelicidin antimicrobial peptide Homo sapiens 73-77 24657252-5 2014 After treatment of cells with exogenous cAMP, forskolin (an activator of cAMP) or KH-7 (an inhibitor of cAMP), respectively, it was confirmed that cAMP communication from bystander cells to targeted cells could mitigate radiation damage in U739 cells, and this cAMP insufficiency in the bystander cells contributed to the enhancement of bystander apoptosis. Colforsin 46-55 cathelicidin antimicrobial peptide Homo sapiens 73-77 24657252-5 2014 After treatment of cells with exogenous cAMP, forskolin (an activator of cAMP) or KH-7 (an inhibitor of cAMP), respectively, it was confirmed that cAMP communication from bystander cells to targeted cells could mitigate radiation damage in U739 cells, and this cAMP insufficiency in the bystander cells contributed to the enhancement of bystander apoptosis. Colforsin 46-55 cathelicidin antimicrobial peptide Homo sapiens 73-77 22723333-6 2012 Western blot analysis using primary antibodies for the phosphorylated cAMP-responsive element (CRE)-binding protein showed markedly reduced CRE-binding protein phosphorylation in the forskolin-stimulated lymphoblastoid cell lines of this patient. Colforsin 183-192 cathelicidin antimicrobial peptide Homo sapiens 70-74 22178870-8 2011 In addition, in CPVT1-cardiomyocytes the Ca(2+)-induced Ca(2+)-release events continued after repolarization and were abolished by increasing the cytosolic cAMP levels with forskolin. Colforsin 173-182 cathelicidin antimicrobial peptide Homo sapiens 156-160 20675307-4 2010 The AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR; 1 mM), and cAMP activators forskolin (10 muM) and cholera toxin (200 ng/ml) also displayed the same effects. Colforsin 140-149 cathelicidin antimicrobial peptide Homo sapiens 124-128 20512473-9 2010 Moreover, CRE promoter activity was dose-dependently inhibited by PAO and the increased secretion of IL-12p40 by PAO was reduced by forskolin, a cAMP activator. Colforsin 132-141 cathelicidin antimicrobial peptide Homo sapiens 145-149 19472214-5 2009 These effects were reversed by addition of forskolin/rolipram (F/R) to increase intracellular cAMP but not by the cAMP analogue 8-pCPT-2"-O-Methyl-cAMP (O-Me-cAMP) which primarily stimulates protein kinase A (PKA)-independent signaling via Epac/Rap 1. Colforsin 43-52 cathelicidin antimicrobial peptide Homo sapiens 94-98 20460737-7 2010 Accumulation of cAMP could be induced by cAMP-elevating agents (forskolin, isobutylmethylxanthine and mastparan) but was not reduced by treatment with C(2)-ceramide. Colforsin 64-73 cathelicidin antimicrobial peptide Homo sapiens 16-20 20460737-7 2010 Accumulation of cAMP could be induced by cAMP-elevating agents (forskolin, isobutylmethylxanthine and mastparan) but was not reduced by treatment with C(2)-ceramide. Colforsin 64-73 cathelicidin antimicrobial peptide Homo sapiens 41-45 19850345-8 2009 To understand whether the inhibitory effect of thymulin on cytokine release is cAMP-dependent, Forskolin, a labdane diterpene known to elevate intracellular cAMP, was shown to reduce the secretion of IL-1beta and TNF-alpha, but not IL-6, an effect mimicked by dibutyryl-cAMP (dbcAMP), an analog of cAMP. Colforsin 95-104 cathelicidin antimicrobial peptide Homo sapiens 79-83 19850345-8 2009 To understand whether the inhibitory effect of thymulin on cytokine release is cAMP-dependent, Forskolin, a labdane diterpene known to elevate intracellular cAMP, was shown to reduce the secretion of IL-1beta and TNF-alpha, but not IL-6, an effect mimicked by dibutyryl-cAMP (dbcAMP), an analog of cAMP. Colforsin 95-104 cathelicidin antimicrobial peptide Homo sapiens 157-161 19850345-8 2009 To understand whether the inhibitory effect of thymulin on cytokine release is cAMP-dependent, Forskolin, a labdane diterpene known to elevate intracellular cAMP, was shown to reduce the secretion of IL-1beta and TNF-alpha, but not IL-6, an effect mimicked by dibutyryl-cAMP (dbcAMP), an analog of cAMP. Colforsin 95-104 cathelicidin antimicrobial peptide Homo sapiens 157-161 19850345-8 2009 To understand whether the inhibitory effect of thymulin on cytokine release is cAMP-dependent, Forskolin, a labdane diterpene known to elevate intracellular cAMP, was shown to reduce the secretion of IL-1beta and TNF-alpha, but not IL-6, an effect mimicked by dibutyryl-cAMP (dbcAMP), an analog of cAMP. Colforsin 95-104 cathelicidin antimicrobial peptide Homo sapiens 157-161 18392843-3 2008 In human dermal microvascular endothelial cells (HDMEC), treatment with forskolin/rolipram (F/R) to increase cAMP by as well as the Epac/Rap 1-stimulating cAMP analogue 8-pCPT-2"-O-methyl-cAMP (O-Me-cAMP) stabilized endothelial barrier properties as revealed by raised transendothelial electrical resistance (TER). Colforsin 72-81 cathelicidin antimicrobial peptide Homo sapiens 109-113 19423690-7 2009 PTH (1 to 31) and forskolin, which activate the cAMP pathway, mimicked the stimulation of TRPV5 activity. Colforsin 18-27 cathelicidin antimicrobial peptide Homo sapiens 48-52 19261611-8 2009 In contrast, cAMP-elevating agents such as PGE(1) and forskolin-induced phosphorylation of Ser(312) and increased PDE3A activity, but did not stimulate 14-3-3 binding. Colforsin 54-63 cathelicidin antimicrobial peptide Homo sapiens 13-17 17586724-3 2007 WAY-132983 also activated the M(4) receptor, fully inhibiting forskolin-induced increase in cAMP levels (IC(50) = 10.5 nM); at the M(2) receptor its potency was reduced by 5-fold (IC(50) = 49.8 nM). Colforsin 62-71 cathelicidin antimicrobial peptide Homo sapiens 92-96 17990294-11 2008 Interestingly, treatment with Wnt3a markedly reduced the forskolin-induced expression of receptor activator of NF-kappaB ligand (RANKL), a target gene of PTH/cAMP/PKA. Colforsin 57-66 cathelicidin antimicrobial peptide Homo sapiens 158-162 17888871-5 2007 This short-term estrogen treatment also significantly enhanced forskolin stimulated cAMP production when compared with the ratio of cAMP/Total measured in cells stimulated with forskolin alone. Colforsin 63-72 cathelicidin antimicrobial peptide Homo sapiens 84-88 17888871-6 2007 Pre-treating MCF7 cells with the same concentration of estrogen for 24h before the assay, on the contrary, significantly decreased the basal cAMP level and it also suppressed cAMP production stimulated with forskolin when compared with its respective value under short-term estrogen treatment. Colforsin 207-216 cathelicidin antimicrobial peptide Homo sapiens 175-179 17320350-7 2007 We found that cAMP/PKA/CREB pathway is indeed an important regulator of Smac/DIABLO transcription, since exposure to the cAMP analog 8-CPT-cAMP, the adenylyl cyclase activator forskolin, the inhibitor of phosphodiesterase isobutylmethylxanthine or by hindering PKA activation with H89, regulated the promoter activity, as shown by gene reporter and RT-PCR assays. Colforsin 176-185 cathelicidin antimicrobial peptide Homo sapiens 14-18 17320350-7 2007 We found that cAMP/PKA/CREB pathway is indeed an important regulator of Smac/DIABLO transcription, since exposure to the cAMP analog 8-CPT-cAMP, the adenylyl cyclase activator forskolin, the inhibitor of phosphodiesterase isobutylmethylxanthine or by hindering PKA activation with H89, regulated the promoter activity, as shown by gene reporter and RT-PCR assays. Colforsin 176-185 cathelicidin antimicrobial peptide Homo sapiens 121-125 17320350-7 2007 We found that cAMP/PKA/CREB pathway is indeed an important regulator of Smac/DIABLO transcription, since exposure to the cAMP analog 8-CPT-cAMP, the adenylyl cyclase activator forskolin, the inhibitor of phosphodiesterase isobutylmethylxanthine or by hindering PKA activation with H89, regulated the promoter activity, as shown by gene reporter and RT-PCR assays. Colforsin 176-185 cathelicidin antimicrobial peptide Homo sapiens 121-125 17097801-8 2007 This effect was enhanced when cAMP levels were increased by forskolin (the maximal effect was 53.0+/-5.1 vs. 83.1+/-5.7%, p<0.01) or in strips with urothelium. Colforsin 60-69 cathelicidin antimicrobial peptide Homo sapiens 30-34 17156132-4 2007 Forskolin is able to decrease the I(K) amplitude recording from neurons of both the LK-S and control group, and prevents apoptosis of granule cells that are induced by LK-S. Dibutyryl cAMP mimicks the effect of forskolin on the modulation of I(K) and, accordingly, the inhibitor of protein kinase A, H-89, aborts the neuron-protective effect induced by forskolin. Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 184-188 17156132-4 2007 Forskolin is able to decrease the I(K) amplitude recording from neurons of both the LK-S and control group, and prevents apoptosis of granule cells that are induced by LK-S. Dibutyryl cAMP mimicks the effect of forskolin on the modulation of I(K) and, accordingly, the inhibitor of protein kinase A, H-89, aborts the neuron-protective effect induced by forskolin. Colforsin 211-220 cathelicidin antimicrobial peptide Homo sapiens 184-188 17156132-4 2007 Forskolin is able to decrease the I(K) amplitude recording from neurons of both the LK-S and control group, and prevents apoptosis of granule cells that are induced by LK-S. Dibutyryl cAMP mimicks the effect of forskolin on the modulation of I(K) and, accordingly, the inhibitor of protein kinase A, H-89, aborts the neuron-protective effect induced by forskolin. Colforsin 353-362 cathelicidin antimicrobial peptide Homo sapiens 184-188 16177565-3 2005 Forskolin, an activator of adenylate cyclase, inhibited fetal bovine serum (FBS)-stimulated BEL-7402 cell proliferation in a dose- and time-dependent manner, along with the inhibition of FBS-stimulated serine/threoine protein kinase Akt (also known as PKB) phosphorylation which is required for Akt activation and this effect was mimicked by 8-Br cAMP. Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 347-351 14602552-7 2003 Forskolin (adenylate cyclase activator) and sodium nitroprusside (SNP, NO donor) resulted in the VASP phosphorylation, with increase in the cAMP and cGMP level, respectively. Colforsin 0-9 cathelicidin antimicrobial peptide Homo sapiens 140-144