PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 1850108-9 1991 When Sertoli cells were incubated with 8-(4-chlorophenylthio) cAMP and cycloheximide, a potent inhibitor of protein synthesis, we observed a super-induction of the mRNAs for c-fos (10-fold) and RI alpha (2-fold). Cycloheximide 71-84 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 174-179 1628615-5 1992 Thirdly, the recently described capacity to act positively as nuclear signalling agonists to stimulate pp33/pp15 phosphorylation is restricted to compounds such as anisomycin and cycloheximide; these, but not emetine or puromycin, will induce c-fos/c-jun on their own. Cycloheximide 179-192 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 243-248 1545132-7 1992 Most of the AP-1 activity could be eliminated when the anti-AIM mAb was added to the culture medium in the presence of cycloheximide, suggesting that de novo protein synthesis is crucial for the induction of AP-1-binding activity. Cycloheximide 119-132 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 12-16 1545132-7 1992 Most of the AP-1 activity could be eliminated when the anti-AIM mAb was added to the culture medium in the presence of cycloheximide, suggesting that de novo protein synthesis is crucial for the induction of AP-1-binding activity. Cycloheximide 119-132 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 208-212 1946467-6 1991 The p53-mediated repression of c-fos gene expression occurred even in the presence of cycloheximide. Cycloheximide 86-99 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 31-36 1704120-3 1991 C-fos in SMS-SB cells can still be induced by serum, TPA and the calcium ionophore, A23187, and superinduced by the combination of serum and cycloheximide. Cycloheximide 141-154 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 2538821-6 1989 We also identified another early gene, F9, whose expression is stimulated upon starvation, is not responsive to cAMP, and is hyperstimulated by cycloheximide, in a manner similar to the cycloheximide stimulation of c-fos and other serum-induced genes in mammalian cells. Cycloheximide 186-199 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 215-220 1702972-11 1990 Previous studies of c-fos RNA from HeLa cells indicate that this is due to cycloheximide-dependent stabilization of poly(A) tails. Cycloheximide 75-88 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 20-25 2739725-4 1989 We now report that a synthetic copy of the c-fos SRE is sufficient to confer cycloheximide-dependent inducibility upon a heterologous promoter. Cycloheximide 77-90 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 43-48 2492191-4 1989 Cycloheximide potentiated the c-fos induction by both EGF and antibody. Cycloheximide 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 3104528-5 1987 Expression of c-fos in PMN was superinduced by exposure to cycloheximide. Cycloheximide 59-72 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-19 2463066-6 1988 The blockade of c-fos gene expression seen in antisense-cells could be caused by rapid degradation of the c-fos message, since c-fos mRNA expression was rescued in these cells when treated with protein synthesis inhibitor, cycloheximide. Cycloheximide 223-236 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-21 2463066-6 1988 The blockade of c-fos gene expression seen in antisense-cells could be caused by rapid degradation of the c-fos message, since c-fos mRNA expression was rescued in these cells when treated with protein synthesis inhibitor, cycloheximide. Cycloheximide 223-236 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-111 2463066-6 1988 The blockade of c-fos gene expression seen in antisense-cells could be caused by rapid degradation of the c-fos message, since c-fos mRNA expression was rescued in these cells when treated with protein synthesis inhibitor, cycloheximide. Cycloheximide 223-236 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-111 2454869-7 1988 Cycloheximide treatment led to induction of a large amount of c-fos mRNA in clones expressing c-fos antisense RNA as well as in control F9 clones. Cycloheximide 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 62-67 2454869-7 1988 Cycloheximide treatment led to induction of a large amount of c-fos mRNA in clones expressing c-fos antisense RNA as well as in control F9 clones. Cycloheximide 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 94-99 2454869-8 1988 The amount of c-fos antisense RNA was also increased by cycloheximide treatment. Cycloheximide 56-69 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-19 2454869-9 1988 We postulate that c-fos antisense RNA blocks expression of the endogenous c-fos gene by accelerating the degradation of c-fos mRNA and that cycloheximide treatment interferes with this degradation. Cycloheximide 140-153 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 74-79 2454869-9 1988 We postulate that c-fos antisense RNA blocks expression of the endogenous c-fos gene by accelerating the degradation of c-fos mRNA and that cycloheximide treatment interferes with this degradation. Cycloheximide 140-153 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 74-79 3316977-7 1987 Cycloheximide was also shown to significantly increase the c-fos mRNA level in HeLa cells. Cycloheximide 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 59-64 3316977-8 1987 There results are consistent with the observation that these inducers of the heat shock response, as well as cycloheximide, repress protein synthesis and suggest that the increase in the level of c-fos mRNA is caused by an inhibition of protein synthesis. Cycloheximide 109-122 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 196-201 3107751-3 1987 This specific increase of c-fos steady-state levels is dependent on the incubation time with a maximal level of induction (over 40-fold) after approximately 1 h. The accumulation of c-fos transcripts is suppressed by alpha-amanitin while cycloheximide intensifies induction only moderately. Cycloheximide 238-251 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 26-31 3103102-6 1987 Treatment of cells with cycloheximide stabilizes c-fos mRNA. Cycloheximide 24-37 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 49-54 3135483-7 1988 (Bu)2cAMP treatment led to a sustained induction of c-fos mRNA, with increased mRNA levels being maintained after 12 h. The FSH-dependent induction of c-fos mRNA was still present in cells treated for 3 h with cycloheximide, but it was greatly reduced by actinomycin D pretreatment. Cycloheximide 210-223 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 52-57 3135483-7 1988 (Bu)2cAMP treatment led to a sustained induction of c-fos mRNA, with increased mRNA levels being maintained after 12 h. The FSH-dependent induction of c-fos mRNA was still present in cells treated for 3 h with cycloheximide, but it was greatly reduced by actinomycin D pretreatment. Cycloheximide 210-223 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 151-156 22358442-4 1987 The expression of c-fos by PMN was superinduced by cycloheximide. Cycloheximide 51-64 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 18-23 3497923-4 1987 A similar rapid increase in c-fos and c-myc mRNA was seen in quiescent FS-4 cells exposed to cycloheximide. Cycloheximide 93-106 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-33 3497813-7 1987 Both c-fos and c-myc mRNA expression were super-induced by the addition of cycloheximide. Cycloheximide 75-88 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 5-10 3032180-9 1987 Moreover, in serum starved cells simultaneously stimulated by serum and infected, only the 2.2 kb fos transcript can be superinduced by the protein synthesis inhibitor cycloheximide, while the appearance of the 4.5 kb fos mRNA is completely blocked by this treatment. Cycloheximide 168-181 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-101 4062932-4 1985 Previous results in the literature have shown that 2 other oncogenes, c-myc and c-fos, can be induced by growth factors in the presence of cycloheximide. Cycloheximide 139-152 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 80-85 3540941-4 1986 Cycloheximide treatment in combination with insulin or phorbol 12-myristate 13-acetate resulted in superinduction of c-fos mRNA. Cycloheximide 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 117-122 3085953-4 1986 Superinduction of c-fos in the presence of cycloheximide occurs primarily because of stabilization of c-fos mRNA. Cycloheximide 43-56 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 18-23 3085953-4 1986 Superinduction of c-fos in the presence of cycloheximide occurs primarily because of stabilization of c-fos mRNA. Cycloheximide 43-56 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 102-107 15136564-2 2004 c-Fos, a component of the AP-1 transcription factor, is transiently induced by H2O2 and the induction is sensitive to the protein synthesis inhibitor cycloheximide. Cycloheximide 150-163 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 3881183-7 1985 Presence of cycloheximide leads to superinduction of c-fos mRNA transcripts. Cycloheximide 12-25 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-58 9822695-6 1998 Inhibition of transcription with actinomycin D and inhibition of protein synthesis with cycloheximide significantly abrogated the effect of UVB on AP-1 DNA binding, indicating that transcription and translation were required for AP-1 activation. Cycloheximide 88-101 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-151 12802426-1 2003 Accumulation of c-fos gene locus DNA in the nuclear matrix of hepatocyte nuclei was observed during induction of c-fos with cycloheximide. Cycloheximide 124-137 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-21 12802426-1 2003 Accumulation of c-fos gene locus DNA in the nuclear matrix of hepatocyte nuclei was observed during induction of c-fos with cycloheximide. Cycloheximide 124-137 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-118 12670444-7 2003 The up-regulation of c-Fos, GATA-1 and NF-E2 protein by PDGF was inhibited by actinomycin D and cycloheximide, suggesting that mRNA and protein synthesis might be involved in the mechanism. Cycloheximide 96-109 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 9822695-6 1998 Inhibition of transcription with actinomycin D and inhibition of protein synthesis with cycloheximide significantly abrogated the effect of UVB on AP-1 DNA binding, indicating that transcription and translation were required for AP-1 activation. Cycloheximide 88-101 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 229-233 9526053-3 1998 Pretreatment with cycloheximide prevented the induction of FOS, but not CREB phosphorylation, normally seen in response to acute ether exposure, and significantly attenuated the stress-induced rise in AVP, but not CRF, heteronuclear RNA expression in the parvocellular division of the PVH. Cycloheximide 18-31 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 59-62 9650640-6 1998 CdCl2 (10 microM) caused an accumulation of c-fos mRNA over 30 min that was sustained for at least 8 h. Cycloheximide inhibits turnover of c-fos mRNA and shows a synergistic effect with Cd2+ on transcript levels. Cycloheximide 104-117 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 44-49 9650640-6 1998 CdCl2 (10 microM) caused an accumulation of c-fos mRNA over 30 min that was sustained for at least 8 h. Cycloheximide inhibits turnover of c-fos mRNA and shows a synergistic effect with Cd2+ on transcript levels. Cycloheximide 104-117 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 139-144 9501479-3 1998 Treatment of C. parasitica with low levels of the protein synthesis inhibitor cycloheximide caused cpc-1 transcript levels to undergo a rapid, transient increase similar to that reported for the mammalian b-ZIP transactivators, c-Jun and c-Fos. Cycloheximide 78-91 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 238-243 8985116-8 1996 In freshly isolated cells, both FOS and FOSB mRNAs increase dramatically in response to the protein synthesis inhibitor cycloheximide. Cycloheximide 120-133 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 32-35 9369245-1 1997 Cycloheximide in sublethal doses caused apoptosis in liver cells in vivo, inducing c-myc, c-fos, c-jun and p53 genes and accumulation of sphingosine, a toxic product of the sphingomyelin cycle. Cycloheximide 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-95 8908616-7 1996 Inhibition of de novo protein synthesis with cycloheximide increased c-fos mRNA stability but not abrogated PGJ2-induced c-fos transcription. Cycloheximide 45-58 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 69-74 8544401-3 1995 The purpose of these studies was (1) to determine whether c-fos is expressed as part of a typical immediate-early (IE) gene response, which would require co-expression of c-jun and sensitivity to cycloheximide, and (2) to determine whether the cells expressing c-Fos are the same as those undergoing DNA synthesis. Cycloheximide 196-209 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-63 8544401-5 1995 c-jun and c-fos mRNA were rapidly and briefly expressed following renal ischemia and their expression was superinduced by cycloheximide in a manner typical of an immediate-early gene response. Cycloheximide 122-135 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 10-15 8764176-6 1996 At both sites, c-fos expression was transient, prolonged by cycloheximide, and was strongly stimulated even in the presence of indomethacin. Cycloheximide 60-73 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-20 8650251-6 1996 The accumulation of c-fos; mRNA in the cultured mammary tissues was also increased by human GH, recombinant bovine PRL, cycloheximide, and phorbol 12-myristate 13-acetate (TPA). Cycloheximide 120-133 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 20-25 8536642-0 1996 Acute nuclear actions of growth hormone (GH): cycloheximide inhibits inducible activator protein-1 activity, but does not block GH-regulated signal transducer and activator of transcription activation or gene expression. Cycloheximide 46-59 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-98 8536642-6 1996 By contrast, CHX completely inhibits the induction of activator protein-1 DNA-binding activity by GH, indicating that this action is secondary to the stimulation of Fos and/or Jun protein biosynthesis. Cycloheximide 13-16 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 54-73 8536642-6 1996 By contrast, CHX completely inhibits the induction of activator protein-1 DNA-binding activity by GH, indicating that this action is secondary to the stimulation of Fos and/or Jun protein biosynthesis. Cycloheximide 13-16 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-168 8690026-7 1995 The treatment of EUE cells with cycloheximide led to superinduction of c-fos expression, (with high levels up to 12 h), and to a c-jun expression that was just detectable. Cycloheximide 32-45 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 71-76 8226882-1 1993 Incubation with 1 nM triiodothyronine (T3) decreased cycloheximide-induced c-fos mRNA levels and the mRNA response to the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 100 nM) or to forskolin (15 microM). Cycloheximide 53-66 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 75-80 7721958-9 1995 In the presence of cycloheximide, TGF-beta causes super-induction of c-fos mRNA at 30 min, indicating that the c-fos expression by TGF-beta is independent of new protein synthesis. Cycloheximide 19-32 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 69-74 7721958-9 1995 In the presence of cycloheximide, TGF-beta causes super-induction of c-fos mRNA at 30 min, indicating that the c-fos expression by TGF-beta is independent of new protein synthesis. Cycloheximide 19-32 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 111-116 8115044-7 1993 Following superinduction of c-fos gene by osmotic stimulation plus cycloheximide treatment, a conspicuous Fos-like immunoreactivity was detected in dispersed chromatin regions, whereas the heterochromatin masses, nucleoli and coiled bodies showed no immunoreaction. Cycloheximide 67-80 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-33 8115044-7 1993 Following superinduction of c-fos gene by osmotic stimulation plus cycloheximide treatment, a conspicuous Fos-like immunoreactivity was detected in dispersed chromatin regions, whereas the heterochromatin masses, nucleoli and coiled bodies showed no immunoreaction. Cycloheximide 67-80 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-109 8115044-9 1993 Since Fos proteins are known to be short-lived, the expression of these nuclear constituents, under conditions of protein synthesis inhibition induced by the cycloheximide, suggests the stabilization of chromatin-bound Fos complexes or, alternatively, a preferential synthesis of Fos proteins. Cycloheximide 158-171 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 219-222 8115044-9 1993 Since Fos proteins are known to be short-lived, the expression of these nuclear constituents, under conditions of protein synthesis inhibition induced by the cycloheximide, suggests the stabilization of chromatin-bound Fos complexes or, alternatively, a preferential synthesis of Fos proteins. Cycloheximide 158-171 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 219-222 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. Cycloheximide 160-173 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 99-104