PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9191080-2 1997 Four days of ethanol exposure enhanced carbachol-stimulated c-fos mRNA expression, analyzed with Northern blot, and Fos/AP-1 binding activity, measured with gel mobility super shift assay. Carbachol 39-48 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 60-65 15893601-0 2005 From synapse to gene product: prolonged expression of c-fos induced by a single microinjection of carbachol in the pontomesencephalic tegmentum. Carbachol 98-107 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 54-59 15893601-6 2005 These results demonstrate a sustained c-fos expression in response to pharmacological stimulation of the brain and suggest that carbachol"s acute effects induce LTPE via cholinergic receptors, with subsequent transsynaptic activation of the LDT/PPT maintaining the LTPE effect. Carbachol 128-137 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-43 11259766-0 2001 Intracerebroventricular carbachol induces FOS immunoreactivity in lamina terminalis neurons projecting to the supraoptic nucleus. Carbachol 24-33 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 42-45 9523591-2 1998 Stimulation with carbachol induced expression of c-fos, fosB, c-jun, junB, and junD. Carbachol 17-26 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 49-54 9523591-6 1998 Inhibition of protein kinase C with GF109203X suppressed the carbachol-stimulated increase in mRNA levels of c-fos, fosB, and junB by approximately 70% but had only minor effects on the expression of c-jun and junD. Carbachol 61-70 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 109-114 9523591-8 1998 Simultaneous inhibition of both protein kinase C and Ca2+/calmodulin-dependent kinase II completely abolished the carbachol-stimulated expression of c-jun and junD, but c-fos, fosB, and junB were still expressed to a certain extent under this condition. Carbachol 114-123 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 169-174 9191080-3 1997 Pre-incubation with muscarinic antagonists or the protein kinase C inhibitor GF109203X demonstrated that, in both control and ethanol-treated cells, carbachol-induced c-fos expression was mediated via muscarinic M1 receptors and to a large extent through protein kinase C. However, phorbol ester-induced c-fos expression was unaffected in ethanol-treated cells. Carbachol 149-158 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 304-309 9191080-4 1997 Acute exposure to ethanol caused a suppression of both carbachol- and phorbol ester-stimulated c-fos expression. Carbachol 55-64 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 95-100 9191080-3 1997 Pre-incubation with muscarinic antagonists or the protein kinase C inhibitor GF109203X demonstrated that, in both control and ethanol-treated cells, carbachol-induced c-fos expression was mediated via muscarinic M1 receptors and to a large extent through protein kinase C. However, phorbol ester-induced c-fos expression was unaffected in ethanol-treated cells. Carbachol 149-158 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-172 8046453-4 1994 In the present experiments we use extracellular recording and immunocytochemistry for Fos, the protein product of c-fos, to demonstrate the activation of the cells following intracerebroventricular administration of the muscarinic agonist, carbachol. Carbachol 240-249 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-89 9037533-0 1996 Carbachol stimulates c-fos expression and proliferation in oligodendrocyte progenitors. Carbachol 0-9 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 9037533-2 1996 Using Northern blot analysis we showed that carbachol caused a time and concentration-dependent increase in c-fos mRNA. Carbachol 44-53 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 108-113 9037533-8 1996 Induction of c-fos mRNA by carbachol was dependent on both influx of extracellular Ca2+ and release from intracellular stores, as both EDTA and BAPTA blocked the response. Carbachol 27-36 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18 8046453-4 1994 In the present experiments we use extracellular recording and immunocytochemistry for Fos, the protein product of c-fos, to demonstrate the activation of the cells following intracerebroventricular administration of the muscarinic agonist, carbachol. Carbachol 240-249 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-119 8046453-5 1994 Fos expression following carbachol injection was then compared with that induced by a similar number of antidromically evoked action potentials. Carbachol 25-34 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-3 18828925-13 2008 Double labeling demonstrated that a number of AVP- and OT-containing neurons in the fetal SON and PVN were expressing c-fos in response to central carbachol. Carbachol 147-156 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-123 7925609-1 1994 In this study, the signal cascade transducing carbachol stimulation into c-fos expression in SH-SY5Y neuroblastoma cells was investigated. Carbachol 46-55 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-78 7925609-3 1994 Application of 1,2-dioctanoylglycerol induced c-fos expression and this, as well as carbachol-stimulated c-fos expression, was inhibited by protein kinase C inhibitors. Carbachol 84-93 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-110 7925609-6 1994 The carbachol-stimulated c-fos expression was potentiated by application of the protein phosphatase inhibitor okadaic acid. Carbachol 4-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 25-30 8974323-5 1994 Stimulation with CCh also induced expression of the immediate-early gene c-fos in these cells. Carbachol 17-20 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-78 7748314-6 1993 Carbachol (1 mM) induced a maximal c-fos mRNA response after 40 minutes in SH-SY5Y cells, an effect that could be mimicked through protein kinase C stimulation by phorbol esters. Carbachol 0-9 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 35-40 1328861-5 1992 Carbachol and thrombin have similar effects on expression of c-fos, fosB, fra-2, junB, and junD, both acutely and over a 24-h time course. Carbachol 0-9 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 61-66 3495533-2 1987 PMA, carbachol, and EGF all stimulated rapid accumulation of mRNA for the proto-oncogenes c-fos and c-myc in the normal cells; in the protein kinase C-deficient cells, carbachol and EGF, but not PMA, retained this effect, which was not mimicked by the calcium ionophore A23187. Carbachol 5-14 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-95 3495533-7 1987 We conclude that, in 1321-N1 cells, induction of c-fos and c-myc mRNA can occur through a protein kinase C-dependent pathway and one or more independent pathways, exemplified by the responses to carbachol and EGF in the protein kinase C-deficient cells. Carbachol 195-204 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 49-54 19269274-3 2009 Consequently, we performed a quantitative, regionally-specific analysis of the Fos immunoreactivity of neurons in the POA of the cat during NREM sleep and REM sleep induced by microinjections of carbachol into the nucleus pontis oralis (REMc), as well as during quiet and alert wakefulness. Carbachol 195-204 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-82 8246917-6 1993 The carbachol-elicited loss of m2- and m3-mAChR mRNA was blocked by their corresponding receptor subtype-specific antagonists, AF-DX 116 (m2-selective) and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) (m3-selective), and was concurrent with an increase in c-fos mRNA levels. Carbachol 4-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 268-273 1328861-2 1992 To determine whether the increases in c-fos and c-jun mRNA induced by carbachol and thrombin are sufficient to stimulate AP-1-mediated transactivation, 1321N1 cells were transfected with a reporter carrying two copies of the tetradecanoyl phorbol acetate response element and the firefly luciferase gene. Carbachol 70-79 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-43 1902229-4 1991 Using the stable acetylcholine analog carbachol to activate muscarinic receptors (mAChR) in a glial cell line (1321N1), we show that c-fos and c-jun mRNA levels are transiently increased, reaching a maximum at 30 min after agonist addition. Carbachol 38-47 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 133-138 1902229-5 1991 Experiments in which the actions of carbachol are blocked by adding atropine at various times demonstrate that only 1.5 min of agonist stimulation is needed to give maximal increases in c-fos or c-jun mRNA at 30 min. Carbachol 36-45 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-191 1902229-7 1991 In cells in which protein kinase C has been down-regulated, carbachol no longer stimulates c-fos or c-jun expression, indicating a critical role for protein kinase C in these responses. Carbachol 60-69 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96 17997396-4 2007 The influence of carbachol, a non-specific cholinergic agonist, on locomotor activity, c-fos expression in the SCN, and the activity of this structure has been previously studied. Carbachol 17-26 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 87-92