PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9095470-7 1996 If the cells were perfused with 10(-6) M ouabain or 10(-5) M forskolin, a similar inhibition of the inotropic response was observed 24 h after TNF alpha-exposure. Colforsin 61-70 tumor necrosis factor Rattus norvegicus 143-152 21335064-9 2011 Moreover, electrical stimulation and forskolin, known to increase intracellular cAMP, potentiate the TNFalpha-mediated upregulation of BDNF expression. Colforsin 37-46 tumor necrosis factor Rattus norvegicus 101-109 15481297-13 2004 Forskolin almost completely blocked TNF release stimulated by LPS or ROS. Colforsin 0-9 tumor necrosis factor Rattus norvegicus 36-39 12641353-12 2003 Forskolin administration was associated with release of cyclic AMP from the heart and completely inhibited LPS-stimulated TNF release. Colforsin 0-9 tumor necrosis factor Rattus norvegicus 122-125 12641353-15 2003 Elevating myocardial cyclic AMP with forskolin completely attenuated LPS-stimulated TNF release. Colforsin 37-46 tumor necrosis factor Rattus norvegicus 84-87 10411124-5 1999 Moreover, TSH/forskolin decrease ICAM-1 RNA levels that are maximally induced by two cytokines: 100 ng/mL tumor necrosis factor-alpha (TNF-alpha) or 100 U/ml interferon-gamma (IFN-gamma). Colforsin 14-23 tumor necrosis factor Rattus norvegicus 135-144 10411124-8 1999 TSH or forskolin, in contrast, halved the activity of the full length chimera within 24 hours and significantly suppressed the TNF-alpha and IFN-gamma-induced increase (>50%; p < 0.02). Colforsin 7-16 tumor necrosis factor Rattus norvegicus 127-136 10195701-5 1999 The promoter activity in VSMC was stimulated by TNF alpha and dexamethasone, and was suppressed by 8-bromo-cAMP and forskolin. Colforsin 116-125 tumor necrosis factor Rattus norvegicus 48-57 9806674-7 1998 Pretreatment of the H9c2 cells with ketamine, plus the combination of TNF-alpha and IFN-gamma, inhibited the reduction of ISO or FSK-induced intracellular cAMP accumulation caused by the proinflammatory cytokines alone. Colforsin 129-132 tumor necrosis factor Rattus norvegicus 70-79 9806674-8 1998 These results demonstrate that the combination of the proinflammatory cytokines TNF-alpha and IFN-gamma reduce poststimulation (ISO or FSK) intracellular cAMP accumulation. Colforsin 135-138 tumor necrosis factor Rattus norvegicus 80-89 9417811-5 1997 Like CGRP, the cAMP agonists prostaglandin E2 (PGE2), dibutyryl cAMP (Bt2cAMP) and forskolin inhibit TNF-alpha production by osteoblasts. Colforsin 83-92 tumor necrosis factor Rattus norvegicus 101-110 9231726-6 1997 Furthermore, cyclic AMP-elevating agents (dibutyryl cyclic AMP and forskolin) inhibited TNF-alpha/IL-1beta-induced and LPS-induced iNOS expression and nitrite accumulation. Colforsin 67-76 tumor necrosis factor Rattus norvegicus 88-97 17234961-9 2007 In contrast, increasing concentrations of forskolin (a direct stimulant of adenylate cyclase) and dibutyryl cAMP (a metabolically active membrane-soluble analog of cAMP) completely reversed TNF-alpha-mediated depression, though only in the presence of NMA. Colforsin 42-51 tumor necrosis factor Rattus norvegicus 190-199 17192570-10 2006 Second, we showed that TNF-alpha reduced significantly the forskolin-stimulated LHRH release and that the CB1-r antagonist AM251 (10(-5) M) blocked that inhibition, supporting the hypothesis that TNF-alpha inhibits LHRH release, acting at least in part by activating the endocannabinoid system. Colforsin 59-68 tumor necrosis factor Rattus norvegicus 23-32 17192570-10 2006 Second, we showed that TNF-alpha reduced significantly the forskolin-stimulated LHRH release and that the CB1-r antagonist AM251 (10(-5) M) blocked that inhibition, supporting the hypothesis that TNF-alpha inhibits LHRH release, acting at least in part by activating the endocannabinoid system. Colforsin 59-68 tumor necrosis factor Rattus norvegicus 196-205 12509806-10 2003 In addition, the cAMP elevating agents dibutyryl cAMP and forskolin both abolished LPS-induced TNFalpha release, thus rendering unlikely the possibility that (+)WIN 55,212-2 could ablate TNFalpha release through the inhibition of adenylate cyclase via the G(i)-coupled cannabinoid receptors type 1 and 2. Colforsin 58-67 tumor necrosis factor Rattus norvegicus 95-103 11964604-15 2002 In addition, elevating myocardial cyclic AMP with forskolin also blocked release of TNF-alpha stimulated by HX-XO. Colforsin 50-59 tumor necrosis factor Rattus norvegicus 84-93 11735278-13 2001 Promotion of cAMP generation by either ISP or FSK reduced TNF-alpha production by hypoxic cells. Colforsin 46-49 tumor necrosis factor Rattus norvegicus 58-67 8256656-8 1993 TNF-alpha inhibition of the PTH-stimulated cAMP response was reversed completely by addition of cholera toxin (5 micrograms/ml) and partially by forskolin (10 microM) but not pertussis toxin (100 and 500 ng/ml). Colforsin 145-154 tumor necrosis factor Rattus norvegicus 0-9 1846528-10 1991 In addition, IL-1 beta and TNF synergistically interacted with forskolin to stimulate phospholipase A2 release from the cells. Colforsin 63-72 tumor necrosis factor Rattus norvegicus 27-30 2551266-5 1989 Moreover, TNF-alpha impairs the LH receptor formation induced by forskolin, cholera toxin or 8-Bromo-cAMP, indicating that the cytokine also acts at a step distal to FSH receptor and to cAMP formation. Colforsin 65-74 tumor necrosis factor Rattus norvegicus 10-19 1648497-4 1991 Furthermore, while noradrenaline exposure led to a decrease in receptor-dependent and -independent adenylyl cyclase activity, treatment of cardiomyocytes with TNF alpha caused a concentration-dependent increase in cyclase responsiveness to either forskolin, guanosine 5"-O-(3-thiotriphosphate) or isoproterenol, even though beta-adrenoceptor density was decreased by TNF alpha. Colforsin 247-256 tumor necrosis factor Rattus norvegicus 159-168