PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11101146-6	2000	Temporal profiles of increases in c-fos mRNA by R(+)-SKF-38393 (50 microM) and forskolin (50 microM) were similar to that of dopamine.	Colforsin	79-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39	
11561718-0	2001	Differential effects of forskolin and phobol 12-myristate-13-acetate on the c-fos and c-jun mRNA expression in rat C6 glioma cells.	Colforsin	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81	
11561718-1	2001	The effects of forskolin (FSK) and phobol 12-myristate-13-acetate (PMA) on c-fos and c-jun mRNA expressions in rat C6 glioma cells were studied.	Colforsin	26-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80	
11561718-2	2001	Both FSK and PMA increased the c-fos mRNA level.	Colforsin	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36	
11561718-4	2001	The elevated c-fos mRNA level, induced by FSK or PMA, was significantly inhibited by dexamethasone (DEX).	Colforsin	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18	
11561718-6	2001	Cycloheximide (CHX) caused a superinduction of the FSK- or PMA-induced c-fos mRNA level.	Colforsin	51-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76	
11561718-13	2001	On-going protein synthesis inhibition is required for the superinduction of the c-fos expression that is induced by PMA, or FSK and the PMA-induced c-jun mRNA level.	Colforsin	124-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85	
11101146-9	2000	However, when cells were treated with dopamine, an increase in the expression of c-Fos immunoreactivity was observed after treatment for 2 h. The treatment of hippocampal neurons with R(+)-SKF38393 (50 microM) or forskolin (50 microM) also induced a significant increase in c-Fos expression.	Colforsin	213-222	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86	
10814831-7	2000	The c-fos mRNA induced by forskolin, but not by NGF, was also suppressed by Puralpha transfection.	Colforsin	26-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9	
10838433-9	1999	Of the compounds tested, only PTH, prostaglandin E(2), 8-bromo-cAMP, and forskolin induced c-fos mRNA levels, indicating that this assay was specific for compounds that are known to induce cAMP and stimulate bone growth.	Colforsin	73-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96	
9879660-4	1998	Treatment of PC12 cells with a combination of agents (NGF, forskolin, and tetradecanoylphorbol acetate [TPA]) increased c-fos expression over that detected with NGF alone.	Colforsin	59-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125	
8756579-3	1996	Although forskolin (5 microM) induced a weak increase in c-fos expression in PD cells, the effect of PT medium conditioned in the presence of forskolin enhanced this expression more than additively (P < 0.05); furthermore, this effect was reversed by melatonin.	Colforsin	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62	
1322332-10	1992	Although both FSH and forskolin activated c-fos and PPenk gene expression in Sertoli cells, the germ cell factor(s) that stimulated PPenk mRNA levels did not affect the expression of this oncogene.	Colforsin	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47	
8926038-6	1995	In contrast to the selective induction of c-fos and junB by CGRP and forskolin, ATP led to the accumulation of all four immediate early genes studied, i.e., c-fos, junB, c-jun, and TIS11.	Colforsin	69-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47	
7891173-6	1995	cAMP analogs and forskolin induced widespread expression of both Fos-like and Fra-like proteins.	Colforsin	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68	
7919167-0	1994	Forskolin increases phosphorylated-CREB and fos immunoreactivity in rat striatum.	Colforsin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47	
7796933-10	1995	The overall study also reveals that among the agonists tested, the dihydropyridine Bay K 8644 and forskolin only were capable to induce a long-lasting stimulation of c-fos and jun B mRNA levels, concomitant to increased levels of PRL transcripts, as does TRH.	Colforsin	98-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171	
7922580-1	1994	We have previously demonstrated that Fos immunoreactivity can be stimulated by KCl, forskolin or glutamate in cultured tyrosine hydroxylase-immunoreactive (TH-ir) hypothalamic neurons.	Colforsin	84-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40	
7922580-6	1994	Pretreatment of the cultures with the D2 agonist LY163502 inhibited KCl- and forskolin-stimulated Fos-ir in TH-ir neurons in a saturable dose-dependent manner.	Colforsin	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101	
7919167-4	1994	Although forskolin did not alter CREB-IR, forskolin did induce striatal P-CREB-IR and Fos-IR by 2.5- and 10-fold, respectively.	Colforsin	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89	
1330491-10	1992	c-fos mRNA was induced by treatment with 50 ng/ml tetradecanoyl phorbol acetate or by 40 ng/ml forskolin, while induction of Egr-1 mRNA was stimulated by treatment with tetradecanoyl phorbol acetate, but not forskolin.	Colforsin	95-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5	
1910045-5	1991	Furthermore, pretreatment of PC12 cells with 20 microM H89, a specific inhibitor of PKA, inhibited forskolin, dibutyryl cAMP, and KCl-induced c-fos and egr1 induction, while having no effect on NGF induction.	Colforsin	99-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147	
3329719-0	1987	Forskolin and a tumor promoter are able to induce c-fos and c-myc expression in normal, but not in a v-ras-transformed rat thyroid cell line.	Colforsin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55	
12106478-7	1991	Agents affecting the intracellular cyclic AMP level, forskolin and Ro 20-1724, stimulated c-fos mRNA in a strong and transient fashion with a temporal sequence similar to the response to CGRP.	Colforsin	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95	
2129102-3	1990	Activation of protein kinase C by phorbol ester lead to increased c-jun and c-fos mRNA levels, whereas activation of adenylate cyclase by forskolin increased c-fos mRNA levels.	Colforsin	138-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163	
3329719-2	1987	c-fos and c-myc oncogenes expression was measured in these cells after addition of their specific growth factor TSH and after treatment with either forskolin, an activator of adenylate cyclase or with a tumor promoter, TPA.	Colforsin	148-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5	
26386156-3	2015	The expression of c-fos was transiently induced by treatment of cells with high potassium (high K(+)), which evoked depolarization, or forskolin, an adenylate cyclase activator.	Colforsin	135-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23	
26386156-4	2015	c-fos expression was persistently and synergistically induced by simultaneous treatment with high K(+) and forskolin via cAMP-response element (CRE).	Colforsin	107-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5	
23047036-5	2012	In ROS17/2.8 cells, FGF2 and FSK each increased the gene expression of c-FOS (7.2-fold and 10.7-fold, respectively).	Colforsin	29-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76	
15155837-6	2004	In cultured smooth muscle cells from rat aorta, forskolin induced a rapid increase in Fos/p-Fos protein levels and activator protein 1 (AP-1) binding activity.	Colforsin	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89	
15155837-6	2004	In cultured smooth muscle cells from rat aorta, forskolin induced a rapid increase in Fos/p-Fos protein levels and activator protein 1 (AP-1) binding activity.	Colforsin	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95	
15155837-8	2004	We conclude that forskolin/cAMP decrease the expression of heterodimeric sGC in rat aortic smooth muscle cells via activation of Fos/AP-1, which decreases the expression of HuR and thus destabilizes the sGCalpha1 and beta1 mRNA.	Colforsin	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132