PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15876423-2 2005 Results of Western blotting show that QE but not its glycoside rutin (RUT) and quicitrin-induced HO-1 protein expression in a time- and dose-dependent manner, and HO-1 protein induced by QE was blocked by an addition of cycloheximide or actinomycin D. Dactinomycin 237-250 heme oxygenase 1 Homo sapiens 163-167 15544924-5 2004 HO-1 mRNA induction was abrogated in the presence of actinomycin D and cycloheximide. Dactinomycin 53-66 heme oxygenase 1 Homo sapiens 0-4 15965068-6 2005 Celecoxib-induced HO-1 protein expression was inhibited by actinomycin D and cycloheximide, suggesting that de novo transcription and translation are required in this process. Dactinomycin 59-72 heme oxygenase 1 Homo sapiens 18-22 15546873-4 2005 The induction of HO-1 by ER stress was blocked by actinomycin D or cycloheximide and was independent of any changes in HO-1 mRNA stability. Dactinomycin 50-63 heme oxygenase 1 Homo sapiens 17-21 12376363-5 2002 Actinomycin D and cycloheximide inhibited TGF-beta1-responsive HO-1 mRNA expression, indicating a requirement for transcription and de novo protein synthesis. Dactinomycin 0-13 heme oxygenase 1 Homo sapiens 63-67 14731112-5 2004 Actinomycin D and cycloheximide inhibited MG132-responsive HO-1 protein expression, indicating a requirement for transcription and de novo protein synthesis. Dactinomycin 0-13 heme oxygenase 1 Homo sapiens 59-63 12036874-3 2002 The induction of HO-1 expression by serum was inhibited by actinomycin D or cycloheximide. Dactinomycin 59-72 heme oxygenase 1 Homo sapiens 17-21 9747510-5 1998 Cycloheximide and actinomycin D inhibited the increases in the HO-1 mRNA level produced by hyperoxia, indicating that response to hyperoxia is dependent on de novo protein synthesis and mRNA transcription. Dactinomycin 18-31 heme oxygenase 1 Homo sapiens 63-67 11592943-9 2001 Coincubation of curcumin with actinomycin D completely blocked the upregulation of HO-1 mRNA. Dactinomycin 30-43 heme oxygenase 1 Homo sapiens 83-87 10872747-13 2000 The increase in HO-1 mRNA was inhibited by actinomycin D and cycloheximide, but not by NAC, and was not mimicked by the lipophilic cGMP analogue, 8-bromo-cGMP, suggesting that NO-mediated induction required de novo RNA and protein synthesis and was unrelated to cGMP and redox signaling. Dactinomycin 43-56 heme oxygenase 1 Homo sapiens 16-20 9808084-7 1998 Treatment with actinomycin-D (4 microM), a transcriptional inhibitor, as well as nuclear run-on assays, demonstrated that LAox-mediated HO-1 gene induction is dependent on de novo transcription. Dactinomycin 15-28 heme oxygenase 1 Homo sapiens 136-140 9784401-4 1998 HO1 levels in LBs treated with arsenite increased by de novo synthesis as demonstrated by incorporation of 35S-methionine and by inhibition of HO1 synthesis by actinomycin D. Dactinomycin 160-173 heme oxygenase 1 Homo sapiens 0-3 9784401-4 1998 HO1 levels in LBs treated with arsenite increased by de novo synthesis as demonstrated by incorporation of 35S-methionine and by inhibition of HO1 synthesis by actinomycin D. Dactinomycin 160-173 heme oxygenase 1 Homo sapiens 143-146 11018038-5 2000 TGF-beta1 treatment in conjunction with actinomycin D or cycloheximide demonstrated that induction of HO-1 mRNA requires de novo transcription and, in part, protein synthesis. Dactinomycin 40-53 heme oxygenase 1 Homo sapiens 102-106 9354392-5 1997 The sodium nitroprusside-mediated increase in heme oxygenase-1 mRNA levels was abolished by treatment with actinomycin D. Dactinomycin 107-120 heme oxygenase 1 Homo sapiens 46-62 16480751-6 2006 Moreover, acrolein-mediated HO-1 induction is abrogated in the presence of actinomycin D and cycloheximide. Dactinomycin 75-88 heme oxygenase 1 Homo sapiens 28-32 8764571-6 1996 The increase in content of heme oxygenase-1 mRNA caused by sodium nitro-prusside was completely abolished by the treatment with actinomycin D. Dactinomycin 128-141 heme oxygenase 1 Homo sapiens 27-43 18332044-5 2008 The Cr(VI)-induced overexpression of heme-oxygenase 1 messenger RNA (HO-1) in the fibroblasts was significantly blocked by actinomycin D and by inhibitors of MAP kinase pathways. Dactinomycin 123-136 heme oxygenase 1 Homo sapiens 37-53 18332044-5 2008 The Cr(VI)-induced overexpression of heme-oxygenase 1 messenger RNA (HO-1) in the fibroblasts was significantly blocked by actinomycin D and by inhibitors of MAP kinase pathways. Dactinomycin 123-136 heme oxygenase 1 Homo sapiens 69-73 17567933-7 2007 Actinomycin D and nuclear run-on studies demonstrate that TGF-beta1 augments HO-1 expression by increased gene transcription and does not involve increased mRNA stability. Dactinomycin 0-13 heme oxygenase 1 Homo sapiens 77-81 26283888-4 2015 Then by analyzing HO-1 mRNA of MG63 cells exposed to ATO in the presence and absence of a transcription inhibitor Actinomycin-D (Act-D), we demonstrated that ATO activates HO-1 expression in MG63 cells by regulating the transcription of the gene. Dactinomycin 114-127 heme oxygenase 1 Homo sapiens 172-176 20974203-10 2011 Because actinomycin D inhibited HO-1 induction by Tg, the induction of HO-1 may be regulated at the transcriptional level. Dactinomycin 8-21 heme oxygenase 1 Homo sapiens 32-36 20974203-10 2011 Because actinomycin D inhibited HO-1 induction by Tg, the induction of HO-1 may be regulated at the transcriptional level. Dactinomycin 8-21 heme oxygenase 1 Homo sapiens 71-75 20594940-6 2010 By contrast, studies with actinomycin D indicated that the half-life of HO-1 mRNA was significantly prolonged in the presence of simvastatin suggesting a post-transcriptional mode of HO-1 regulation. Dactinomycin 26-39 heme oxygenase 1 Homo sapiens 72-76 20594940-6 2010 By contrast, studies with actinomycin D indicated that the half-life of HO-1 mRNA was significantly prolonged in the presence of simvastatin suggesting a post-transcriptional mode of HO-1 regulation. Dactinomycin 26-39 heme oxygenase 1 Homo sapiens 183-187 19653226-5 2009 Actinomycin D (an RNA synthesis inhibitor) and cycloheximide (a protein synthesis inhibitor) inhibited sulforaphane-responsive HO-1 mRNA expression, indicating that sulforaphane is a requirement for transcription and de novo protein synthesis. Dactinomycin 0-13 heme oxygenase 1 Homo sapiens 127-131 16378625-3 2006 Furthermore, EGCG-mediated HO-1 induction was abrogated in the presence of actinomycin D and cycloheximide, indicating that this upregulation of HO-1 occurred at the transcriptional level. Dactinomycin 75-88 heme oxygenase 1 Homo sapiens 27-31 16378625-3 2006 Furthermore, EGCG-mediated HO-1 induction was abrogated in the presence of actinomycin D and cycloheximide, indicating that this upregulation of HO-1 occurred at the transcriptional level. Dactinomycin 75-88 heme oxygenase 1 Homo sapiens 145-149 16537525-7 2006 Actinomycin D inhibited LNO(2) induction of HO-1 in human aortic endothelial cells, and LNO(2) activated a 4.5-kb human HO-1 promoter construct, indicating transcriptional regulation of the HO-1 gene. Dactinomycin 0-13 heme oxygenase 1 Homo sapiens 44-48