PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11098108-8 2000 Prior treatment of the protein synthesis inhibitor cycloheximide prevented the expression of immunoreactivities to the anti-c-Fos antibody detected on two-dimensional electrophoresis in hippocampal nuclear fractions obtained 2h after administration.These results suggest that in vivo kainate signals may lead to persistent expression of the transcription factor activator protein-1 that consists of different Fos family members, as well as of c-Fos protein phosphorylated on serine and/or tyrosine residues, at an early stage after administration. Cycloheximide 51-64 jun proto-oncogene Mus musculus 362-381 10200990-11 1999 Estradiol-enhanced binding of nuclear extracts to the AP-1 oligonucleotide was reversed by cycloheximide. Cycloheximide 91-104 jun proto-oncogene Mus musculus 54-58 10497315-9 1999 Consistent with c-jun, their mRNA expressions were simultaneously superinduced by cycloheximide (1 microg/ml), suggesting that de novo protein synthesis is involved their transcriptions. Cycloheximide 82-95 jun proto-oncogene Mus musculus 16-21 10493750-5 1999 Treatment of muscle cells with cycloheximide to inhibit c-JUN synthesis at the protein level and suppression of c-JUN function by a dominant-negative mutant blocked neuregulin-induced expression of the epsilon-subunit gene, indicating an essential role of c-JUN in neuregulin signaling. Cycloheximide 31-44 jun proto-oncogene Mus musculus 56-61 9749794-4 1998 The protein synthesis inhibitor cycloheximide blocked all these phenomena, whereas RNA synthesis inhibitor actinomycin-D, survival factor such as insulin-like growth factor-1, brain-derived neurotrophic factor, high K+ (25 mM) and overproduced antiapoptotic protein Bcl-2, prevented deltapsi, loss, caspase activation, and nuclear change, but not an increase in active c-Jun. Cycloheximide 32-45 jun proto-oncogene Mus musculus 369-374 9042210-5 1996 Cycloheximide (CHX) treatment of the cells resulted in the increase in the mRNA levels for c-jun, jun B, krox 24 and p53 in the Y-8 and ED2 cell lines. Cycloheximide 0-13 jun proto-oncogene Mus musculus 91-96 9378495-5 1997 Cycloheximide superinduced c-fos and c-jun induction by IFN-gamma, thus indicating that both act as immediate early genes. Cycloheximide 0-13 jun proto-oncogene Mus musculus 37-42 9176392-8 1997 When C3H/HeN mice were pretreated with cycloheximide before hepatectomy, the early peak of Bcl-x mRNA at 4 hours was essentially abrogated whereas the immediate-early gene c-myc was hyperinduced, thus implicating Bcl-x as a delayed early response gene during liver regeneration. Cycloheximide 39-52 jun proto-oncogene Mus musculus 151-166 9042210-5 1996 Cycloheximide (CHX) treatment of the cells resulted in the increase in the mRNA levels for c-jun, jun B, krox 24 and p53 in the Y-8 and ED2 cell lines. Cycloheximide 15-18 jun proto-oncogene Mus musculus 91-96 7822029-9 1995 Cycloheximide inhibited the accumulation of LPS-stimulated IRF-2 and ICSBP mRNA, but not IRF-1 mRNA, thus designating IRF-1 an immediate-early, LPS-inducible gene. Cycloheximide 0-13 jun proto-oncogene Mus musculus 127-142 8649769-2 1996 Okadaic acid increased AP-1 binding to a consensus TPA responsive element (TRE) within 2 h; maximum stimulation was observed at 6 h followed by a gradual decrease to basal levels within 24 h. Jun B, Jun D and Fos B proteins were identified as the major components of the AP-1 complex binding to the TRE element at 6 h. Inhibition of transcription with actinomycin D and inhibition of protein synthesis with cycloheximide abrogated the okadaic acid effect on AP-1 DNA binding, indicating that transcription and translation are required for okadaic acid increased TRE binding activity. Cycloheximide 407-420 jun proto-oncogene Mus musculus 23-27 8012956-5 1994 The kinetics of this transient induction, which is enhanced by cycloheximide, demonstrates that WAF1/CIP1 is an immediate-early gene the transcript of which reaches a peak at approximately 2 h following serum or growth factor stimulation. Cycloheximide 63-76 jun proto-oncogene Mus musculus 112-127 8083371-7 1994 In 3T3 cells, acid activated IE genes by a different mechanism in that the increase in mRNA did not include c-jun, was more prolonged, and was blocked by cycloheximide. Cycloheximide 154-167 jun proto-oncogene Mus musculus 29-31 2123531-6 1990 When protein synthesis is inhibited by injection of cycloheximide, the expression of c-myc, c-fos, jun B, c-jun and jun D mRNA is also transiently increased. Cycloheximide 52-65 jun proto-oncogene Mus musculus 106-111 1456083-4 1992 The addition of serum together with cycloheximide, an inhibitor of protein synthesis, resulted in the superinduction of both c-fos and c-jun mRNAs. Cycloheximide 36-49 jun proto-oncogene Mus musculus 135-140 1550560-2 1992 Cells exposed to cycloheximide and IGF I together showed super-induction of c-jun transcripts. Cycloheximide 17-30 jun proto-oncogene Mus musculus 76-81 2114348-8 1990 C-jun induction occurred with cycloheximide alone, but partial hepatectomy further increased c-jun expression, indicating that new protein synthesis was not required for this effect. Cycloheximide 30-43 jun proto-oncogene Mus musculus 0-5 1696944-6 1990 In the presence of cycloheximide, c-jun and c-myc genes were superinduced by the addition of cadmium. Cycloheximide 19-32 jun proto-oncogene Mus musculus 34-39 1696944-8 1990 Induction of c-myc and c-jun by cadmium and c-fos by a combination of cadmium and cycloheximide could be abolished by blocking transcription with actinomycin D. Cycloheximide 82-95 jun proto-oncogene Mus musculus 23-28 3026286-2 1987 Ten proteins were classified as IE by their time of synthesis and by their synthesis in the presence of actinomycin D following reversal of a cycloheximide mediated protein synthesis block. Cycloheximide 142-155 jun proto-oncogene Mus musculus 32-34 6479164-1 1984 Cycloheximide reversal experiments in chick embryo fibroblasts and mouse L-929 cells indicate that the poxvirus-induced enzymes DNA polymerase and "alkaline" DNase are immediate early gene products of the virus. Cycloheximide 0-13 jun proto-oncogene Mus musculus 168-183 12788213-8 2003 Furthermore, cycloheximide inhibited the increased c-Fos and c-Jun protein expression levels induced by KA in the hippocampus. Cycloheximide 13-26 jun proto-oncogene Mus musculus 61-66 15563689-4 2005 TLR4-activated CD11b expression was cycloheximide sensitive and involved the activation of transcription factors, NF-kappaB and c-Jun/PU.1. Cycloheximide 36-49 jun proto-oncogene Mus musculus 128-133