PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11779361-5 2002 Cycloheximide also inhibited the activation of caspases and AP-1, the expression of Fas, the formation of DISC and the release of cytochrome-C, but not the activation of SAPK/JNK in X-irradiated MOLT-4 cells. Cycloheximide 0-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 60-64 11448101-6 2001 HMBA induces c-fos and represses cycloheximide-induced c-jun and fra-1 expression. Cycloheximide 33-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 55-60 11461775-7 2001 In fact, protein synthesis inhibitor cycloheximide (CHX) prevented the stimulation of AP-1 nuclear binding due to PMA and ascorbate plus PMA. Cycloheximide 37-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90 11461775-7 2001 In fact, protein synthesis inhibitor cycloheximide (CHX) prevented the stimulation of AP-1 nuclear binding due to PMA and ascorbate plus PMA. Cycloheximide 52-55 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90 11226825-5 2000 Use of cycloheximide to block protein synthesis strongly induced c-jun mRNA, suggesting that there had been relief from a labile protein repressor of transcription. Cycloheximide 7-20 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-70 11226825-7 2000 The high induction by cycloheximide obscured simple interpretation of elevated c-jun mRNA levels after concomitant administration of cycloheximide and dexamethasone. Cycloheximide 22-35 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-84 11226825-7 2000 The high induction by cycloheximide obscured simple interpretation of elevated c-jun mRNA levels after concomitant administration of cycloheximide and dexamethasone. Cycloheximide 133-146 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-84 10228559-10 1999 The increase in AP-1 DNA-binding activity and the increase in ERCC-1 mRNA expression were prevented by pretreatment with cycloheximide. Cycloheximide 121-134 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-20 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 97-102 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 228-233 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 129-134 7527398-5 1994 p54 MAP kinase (also called stress-activated protein kinase) is a c-Jun kinase first isolated from livers of cycloheximide-treated rats. Cycloheximide 109-122 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 66-71 1448115-5 1992 Although the c-jun mRNA level was increased by cycloheximide alone, a further 2.4-fold increase was seen when the cells were treated with MPA in the presence of cycloheximide. Cycloheximide 47-60 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18 8395533-0 1993 Interleukin-3 inhibits cycloheximide induction of C-jun mRNA in human monocytes: possible role for a serine/threonine phosphatase. Cycloheximide 23-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 50-55 8395533-1 1993 Cycloheximide is a strong inducer of the c-jun protooncogene mRNA at concentrations (< or = 50 ng/ml) that do not inhibit protein synthesis in human monocytes. Cycloheximide 0-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 41-46 8395533-3 1993 The pluripotent colony stimulating factor interleukin-3 (IL-3) (10 ng/ml) is also a modest inducer of the c-jun gene in these cells; however, in combination with cycloheximide, IL-3 dramatically reduces the c-jun induction below levels induced by cycloheximide alone. Cycloheximide 247-260 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-111 8395533-5 1993 Preincubation of monocytes with 12.5 nM okadaic acid (a potent inhibitor of protein phosphatases 1 and 2A) and cycloheximide prior to addition of IL-3 restored the level of c-jun induction to that mediated by cycloheximide alone. Cycloheximide 111-124 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 173-178 8395533-5 1993 Preincubation of monocytes with 12.5 nM okadaic acid (a potent inhibitor of protein phosphatases 1 and 2A) and cycloheximide prior to addition of IL-3 restored the level of c-jun induction to that mediated by cycloheximide alone. Cycloheximide 209-222 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 173-178 8395533-7 1993 These observations suggest that activation of protein serine/threonine phosphatase(s) underlies the ability of IL-3 to inhibit cycloheximide induction of c-jun in monocytes. Cycloheximide 127-140 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 154-159 1448115-5 1992 Although the c-jun mRNA level was increased by cycloheximide alone, a further 2.4-fold increase was seen when the cells were treated with MPA in the presence of cycloheximide. Cycloheximide 161-174 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 249-254 1419903-5 1992 c-jun mRNA levels were superinduced in cells treated with both okadaic acid and cycloheximide, whereas inhibition of protein synthesis had little, if any, effect on okadaic acid-induced c-jun transcription. Cycloheximide 80-93 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 1419903-7 1992 In contrast, treatment with both okadaic acid and cycloheximide was associated with stabilization (t 1/2 = 90 min) of c-jun transcripts. Cycloheximide 50-63 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-123 2105946-7 1990 TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Cycloheximide 48-61 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 100-105 2144551-10 1990 The protein synthesis inhibitor cycloheximide did not block the induction of any of these genes, and in fact, super-induced the expression of c-jun and hck. Cycloheximide 32-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 142-147 2105946-11 1990 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Cycloheximide 78-91 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 2105946-11 1990 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Cycloheximide 78-91 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 178-183 2542296-2 1989 The c-jun transcripts increase within 15 min after NGF addition, peak at 1 h, and decline to basal level by 4 h. Actinomycin D inhibits the increase, and cycloheximide prevents the decrease of c-jun mRNA. Cycloheximide 154-167 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9 2477086-9 1989 The c-jun transcripts in myelomonocytic cells have a half-life of approximately 20 minutes and are superinduced by cycloheximide, which affects both the degradation rate of mRNA and the transcriptional activity of the c-jun gene. Cycloheximide 115-128 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9 2477086-9 1989 The c-jun transcripts in myelomonocytic cells have a half-life of approximately 20 minutes and are superinduced by cycloheximide, which affects both the degradation rate of mRNA and the transcriptional activity of the c-jun gene. Cycloheximide 115-128 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 218-223 2542296-2 1989 The c-jun transcripts increase within 15 min after NGF addition, peak at 1 h, and decline to basal level by 4 h. Actinomycin D inhibits the increase, and cycloheximide prevents the decrease of c-jun mRNA. Cycloheximide 154-167 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 193-198