PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10764409-7 2000 Forskolin, an activator of adenylyl cyclase, and sodium nitroprusside, an NO donor, increased P-CREB and c-fos levels. Colforsin 0-9 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-110 9710361-8 1998 This response was transient, as the level returned to the control level after 6 h. Forskolin and TPA evoked similar increases, but their effects appeared after 30 min and reached their maxima after 2 h. In contrast, GRF and forskolin, but not TPA, increased the GH mRNA level 2-fold after 24 h. The cJun mRNA level showed no significant change in response to these agents over 24 h and GRF and TPA increased the cFos mRNA level 1.4 and 2.3-fold, respectively, after 30 min. Colforsin 83-92 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 412-416 9517483-5 1997 Overexpression of ICER in cultured spinal cord neurons results in the repression of the c-fos and c-jun promoters induced by forskolin and glutamate. Colforsin 125-134 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 88-93 8760066-3 1996 Using IMR fibroblasts, we found that prostaglandin E1 (PGE1) and forskolin, stimulators of cAMP accumulation in young and senescent cells, increased abundance of c-fos and junB mRNA more in young than senescent cells. Colforsin 65-74 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 162-167 9133371-3 1997 Although glutamate, dopamine, and forskolin (an activator of adenylate cyclase) all induce c-fos mRNA and AP-1 binding, we found, surprisingly, that only glutamate induces transcription of a transfected AP-1-driven fusion gene. Colforsin 34-43 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96 9068120-8 1997 Application of the D1 agonist SKF 38393, or direct stimulation of adenylyl cyclase with forskolin, also resulted in the phosphorylation of CREB and the induction of c-fos in striatal neurons. Colforsin 88-97 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-170 8912813-4 1996 Melatonin was able to significantly inhibit forskolin-stimulated induction of c-fos and jun B mRNA whilst forskolin had no effect upon c-jun or jun D. Colforsin 44-53 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 78-83 8912813-5 1996 Induction of c-Fos translation by forskolin was also inhibited by melatonin. Colforsin 34-43 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18 8793856-4 1996 Reverse transcription-polymerase chain reaction (RT-PCR) analysis was performed to estimate the c-jun and c-fos mRNA contents in GnRH-, forskolin- (cAMP activator) and tetradecanoyl phorbol acetate- (TPA; protein kinase C activator) treated primary cultures of porcine anterior pituitary cells. Colforsin 136-145 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-111 7757250-5 1994 In contrast, forskolin- and A23187-induced c-fos expression and constitutive beta-2 microglobulin expression remain unaffected. Colforsin 13-22 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 43-48 8522361-5 1995 However, kinase C activation (PMA stimulation) combined with either cAMP (forskolin plus MIX) or calcium stimulation (ionophore) leads to greatly enhanced c-fos induction. Colforsin 74-83 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 155-160 7982047-6 1994 Forskolin increased the percentage of Fos/TH-ir neurons in a dose-dependent manner, with a maximal stimulation of 53.4 +/- 4.5% Fos/TH-ir neurons at 30 microM forskolin. Colforsin 0-9 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-41 7982047-6 1994 Forskolin increased the percentage of Fos/TH-ir neurons in a dose-dependent manner, with a maximal stimulation of 53.4 +/- 4.5% Fos/TH-ir neurons at 30 microM forskolin. Colforsin 0-9 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 128-131 7982047-6 1994 Forskolin increased the percentage of Fos/TH-ir neurons in a dose-dependent manner, with a maximal stimulation of 53.4 +/- 4.5% Fos/TH-ir neurons at 30 microM forskolin. Colforsin 159-168 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-41 7982047-6 1994 Forskolin increased the percentage of Fos/TH-ir neurons in a dose-dependent manner, with a maximal stimulation of 53.4 +/- 4.5% Fos/TH-ir neurons at 30 microM forskolin. Colforsin 159-168 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 128-131 1935903-5 1991 Transactivation by the endogenous PR in T47D cells could be inhibited by increasing the intracellular c-Fos level with forskolin as well as by co-expressing c-Fos; no such effect was seen in MCF-7 cells. Colforsin 119-128 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 102-107 8226882-3 1993 In transient transfection assays with a c-fos promoter reporter construct T3 decreased basal promoter activity by more than 50-60% and strongly inhibited the TPA and forskolin-induced activity. Colforsin 166-175 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-45 8226882-6 1993 Retinoic acid (RA) had an effect similar to T3 reducing basal CAT activity and the response to TPA and forskolin by 40-50% in cells co-transfected with the c-fos promoter and an expression vector for the RA receptor. Colforsin 103-112 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 156-161 1335418-4 1992 Both PMA and the combination of NECA and forskolin acted together either to increase (c-Fos) or decrease (Jun) protein levels as well as increasing AP-1 binding, as judged by gel-shift assay, and AP-1 transcriptional activity. Colforsin 41-50 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-91 11536950-6 1992 Under simulated weightlessness conditions EGF- and TPA-induced c-fos expression was decreased, while forskolin- and A23187-induced c-fos expression was independent of the gravity conditions. Colforsin 101-110 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 131-136 7693011-3 1993 Addition of foetal calf serum or forskolin to the medium stimulated basal CCK and c-fos mRNA expression. Colforsin 33-42 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 82-87 7693011-4 1993 Addition of cycloheximide suppressed the stimulation of CCK mRNA expression, whereas expression of c-fos mRNA was super-induced by the simultaneous addition of cycloheximide and forskolin or foetal calf serum. Colforsin 178-187 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 99-104 1545828-2 1992 We demonstrate that the human c-Fos protein, phosphorylated either in vitro with purified PKA or in vivo in JEG3 cells following treatment with forskolin, has similar phosphotryptic peptide maps. Colforsin 144-153 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 1655978-9 1991 Forskolin enhanced the induction of both junB and c-fos mRNA whereas corticosterone prolonged junB mRNA induction. Colforsin 0-9 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 50-55 1915667-3 1991 In this paper we show that epidermal growth factor (EGF)- and 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced expression of the c-fos and c-jun protooncogenes is decreased in microgravity, while no effect of gravity changes was observed on A23187- and forskolin-induced expression of these genes. Colforsin 256-265 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-137 15180304-7 2004 Both phorbol 12-myristate 13-acetate (PMA; 2.5 mM) and forskolin (FSK; 5 mM) increased the c-fos and c-jun mRNA expressions. Colforsin 55-64 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96 3135483-6 1988 The c-fos mRNA was also elevated after treatment of the Sertoli cell with (Bu)2cAMP and forskolin. Colforsin 88-97 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9 1648385-12 1991 The induction of t-PA mRNA by PMA was dependent on protein synthesis and was preceded by a strong transient increase in c-jun and c-fos mRNA levels; the induction of c-fos but not of c-jun was potentiated by forskolin. Colforsin 208-217 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 166-171 1666980-3 1991 We observed that forskolin induced transient expression of the c-fos gene in the presence of a calcium ionophore A23187 in NIH3T3 fibroblasts. Colforsin 17-26 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 63-68 2108403-6 1990 Nuclear expression of the c-fos protein was also induced by veratridine, forskolin and the calcium ionophore A231287. Colforsin 73-82 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 26-31 2511437-5 1989 The 115-base pair (bp) region from -225 to -111 in the IL-6 5"-flanking region, which shares nucleotide sequence similarity with the c-fos serum response (SRE) and adjacent AP-1-like (the CGTCA motif) elements, confers responsiveness to several reagents, including serum, forskolin, and phorbol ester, upon the heterologous herpesvirus thymidine kinase (TK) promoter. Colforsin 272-281 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 133-138 3135482-4 1987 Forskolin and phorbol 12, 13 dibutyrate induced c-fos gene in cultured primary pituitary cells with similar kinetics. Colforsin 0-9 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 48-53 15180304-7 2004 Both phorbol 12-myristate 13-acetate (PMA; 2.5 mM) and forskolin (FSK; 5 mM) increased the c-fos and c-jun mRNA expressions. Colforsin 66-69 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96 12890570-5 2003 Since activities of CRE-luc and c-fos-luc were highly dependent on cell types, GnRH-induced CRE-luc or c-fos-luc activity was normalized by forskolin-induced CRE-luc or 12-O-tetradecanoylphenol-13-acetate (TPA)-induced c-fos-luc activity, respectively. Colforsin 140-149 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 32-37 12890570-5 2003 Since activities of CRE-luc and c-fos-luc were highly dependent on cell types, GnRH-induced CRE-luc or c-fos-luc activity was normalized by forskolin-induced CRE-luc or 12-O-tetradecanoylphenol-13-acetate (TPA)-induced c-fos-luc activity, respectively. Colforsin 140-149 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-108 12890570-5 2003 Since activities of CRE-luc and c-fos-luc were highly dependent on cell types, GnRH-induced CRE-luc or c-fos-luc activity was normalized by forskolin-induced CRE-luc or 12-O-tetradecanoylphenol-13-acetate (TPA)-induced c-fos-luc activity, respectively. Colforsin 140-149 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-108 12372763-5 2002 Selective stimulation of CaMK with Ca(2+) ionophores and of PKA with forskolin or dibutyryl cAMP both result in induction of c-fos mRNA. Colforsin 69-78 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 125-130