PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 3131075-12 1987 Synthesis of TNF is inhibited by actinomycin D or cycloheximide, indicating that it is an inducible protein. Cycloheximide 50-63 tumor necrosis factor Homo sapiens 13-16 33439776-8 2021 Blocking protein synthesis using Cycloheximide prevented Cldn-3 upregulation by TNFalpha, verifying the contribution of de novo Cldn-3 synthesis. Cycloheximide 33-46 tumor necrosis factor Homo sapiens 80-88 3330013-3 1987 When protein synthesis was inhibited by cycloheximide, however, TNF was cytotoxic for all cells except BT-20 cells. Cycloheximide 40-53 tumor necrosis factor Homo sapiens 64-67 3023310-13 1986 The turnover of TNF receptors on HeLA S3 cells seemed to be rapid, since the level of specific binding quickly decreased after treatment with 100 micrograms/ml of cycloheximide at 37 degrees C with a half-life of about 1.5 h. The crosslinking of the cell-bound 125I-TNF with the use of disuccinimidyl suberate yielded a complex of 105 kDa for HeLa S3 and THP-1 cells, and a complex of 100 kDa for U937 cells. Cycloheximide 163-176 tumor necrosis factor Homo sapiens 16-19 3023310-13 1986 The turnover of TNF receptors on HeLA S3 cells seemed to be rapid, since the level of specific binding quickly decreased after treatment with 100 micrograms/ml of cycloheximide at 37 degrees C with a half-life of about 1.5 h. The crosslinking of the cell-bound 125I-TNF with the use of disuccinimidyl suberate yielded a complex of 105 kDa for HeLa S3 and THP-1 cells, and a complex of 100 kDa for U937 cells. Cycloheximide 163-176 tumor necrosis factor Homo sapiens 266-269 30902881-6 2019 Importantly, the loss of cIAP1 enhanced TNF-alpha/cycloheximide-induced apoptosis in higher activation statuses of Caspase-8, Caspase-3 without the induction of Complex II. Cycloheximide 50-63 tumor necrosis factor Homo sapiens 40-49 32354117-7 2020 Furthermore, depletion of USP20 disrupts formation of the atypical PKCzeta-RIPK1-p62 complex required for TNFalpha-mediated NF-kappaB activation and significantly increases the apoptosis induced by TNFalpha plus cycloheximide or TNFalpha plus TAK1 inhibitor. Cycloheximide 212-225 tumor necrosis factor Homo sapiens 106-114 32354117-7 2020 Furthermore, depletion of USP20 disrupts formation of the atypical PKCzeta-RIPK1-p62 complex required for TNFalpha-mediated NF-kappaB activation and significantly increases the apoptosis induced by TNFalpha plus cycloheximide or TNFalpha plus TAK1 inhibitor. Cycloheximide 212-225 tumor necrosis factor Homo sapiens 198-206 28842570-4 2017 Using phospho-Ser321 as a marker, we show that the transient phosphorylation of RIPK1 intermediate domain induced by TNFalpha leads to RIPK1-independent apoptosis when NF-kappaB activation is inhibited by cycloheximide. Cycloheximide 205-218 tumor necrosis factor Homo sapiens 117-125 30566394-5 2019 Apoptosis was induced by addition of tumor necrosis factor-alpha to cycloheximide-sensitized endothelial cells. Cycloheximide 68-81 tumor necrosis factor Homo sapiens 37-64 30566394-7 2019 Our results reveal that proteins of healthy basement membrane alleviate cytokine-induced apoptosis whereas precoating with collagen type I had no significant effect on apoptosis by addition of tumor necrosis factor-alpha to cycloheximide-sensitized endothelial cells compared with cells cultured on uncoated plates. Cycloheximide 224-237 tumor necrosis factor Homo sapiens 193-220 29131527-0 2018 3D matrix-embedding inhibits cycloheximide-mediated sensitization to TNF-alpha-induced apoptosis of human endothelial cells. Cycloheximide 29-42 tumor necrosis factor Homo sapiens 69-78 29398714-1 2018 Abstract: The exposure of HeLa cells to interleukin-1 alpha (IL-1alpha) in the presence of cycloheximide (CHX) leads to the release of active tumor necrosis factor alpha (TNF-alpha), eliciting cytocidal effect on these cells. Cycloheximide 91-104 tumor necrosis factor Homo sapiens 142-169 29398714-1 2018 Abstract: The exposure of HeLa cells to interleukin-1 alpha (IL-1alpha) in the presence of cycloheximide (CHX) leads to the release of active tumor necrosis factor alpha (TNF-alpha), eliciting cytocidal effect on these cells. Cycloheximide 91-104 tumor necrosis factor Homo sapiens 171-180 29398714-1 2018 Abstract: The exposure of HeLa cells to interleukin-1 alpha (IL-1alpha) in the presence of cycloheximide (CHX) leads to the release of active tumor necrosis factor alpha (TNF-alpha), eliciting cytocidal effect on these cells. Cycloheximide 106-109 tumor necrosis factor Homo sapiens 142-169 29398714-1 2018 Abstract: The exposure of HeLa cells to interleukin-1 alpha (IL-1alpha) in the presence of cycloheximide (CHX) leads to the release of active tumor necrosis factor alpha (TNF-alpha), eliciting cytocidal effect on these cells. Cycloheximide 106-109 tumor necrosis factor Homo sapiens 171-180 29162874-6 2017 Simultaneous exposure to TNF or LPS and a translation inhibitor, cycloheximide, leads to prolonged NF-kappaB activation and a marked increase of transcript levels of NF-kappaB inhibitors, IkappaBalpha and A20. Cycloheximide 65-78 tumor necrosis factor Homo sapiens 25-28 26626244-4 2015 RESULTS: The results showed that the numbers of microparticles were increased by tumour necrosis factor (TNF) or the combination of TNF and cycloheximide (CHX). Cycloheximide 155-158 tumor necrosis factor Homo sapiens 132-135 26985709-6 2016 In the current study, BMSCs were treated with TNF-alpha/cycloheximide (CHX), and cell death was examined by the Cell Counting Kit-8, Hoechst 33342 staining, and flow cytometric analysis as well as by the level of caspase-3 and caspase-8. Cycloheximide 71-74 tumor necrosis factor Homo sapiens 46-55 26198031-2 2015 Incubation of human dermal fibroblasts with TAPF (TNF Apoptosis Protection Fraction) protects them from apoptosis induced by the subsequent addition of TNF and cycloheximide (CHX). Cycloheximide 160-173 tumor necrosis factor Homo sapiens 50-53 26198031-2 2015 Incubation of human dermal fibroblasts with TAPF (TNF Apoptosis Protection Fraction) protects them from apoptosis induced by the subsequent addition of TNF and cycloheximide (CHX). Cycloheximide 175-178 tumor necrosis factor Homo sapiens 50-53 25936522-5 2015 In HUVEC depleted of coronin 1A by siRNA transfection, tumor necrosis factor alpha (TNFalpha)+cyclohexamide (CHX) treatment resulted in a decrease in the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive apoptotic cells. Cycloheximide 109-112 tumor necrosis factor Homo sapiens 55-82 27415790-9 2016 Suppression of miR-122 could reduce apoptosis and caspase activity in pterygium epithelial cell treated with TNFalpha/cycloheximide (CHX), and this effect was abolished by inhibition of the expression of Bcl-w with specific siRNA. Cycloheximide 118-131 tumor necrosis factor Homo sapiens 109-117 27415790-9 2016 Suppression of miR-122 could reduce apoptosis and caspase activity in pterygium epithelial cell treated with TNFalpha/cycloheximide (CHX), and this effect was abolished by inhibition of the expression of Bcl-w with specific siRNA. Cycloheximide 133-136 tumor necrosis factor Homo sapiens 109-117 26606373-7 2016 Instead, TNF-alpha-induced COX-2 upregulation is subject to regulation by the proteasome, and IL-17A acts to increase TNF-alpha-induced COX-2 protein stability as confirmed by cycloheximide chase experiments. Cycloheximide 176-189 tumor necrosis factor Homo sapiens 118-127 25148872-1 2014 The present study is aimed to determine the protective effect of a novel nanoparticle with antioxidant properties, nanoceria, on reactive oxygen species (ROS) production, and calcium signaling evoked by the tumor necrosis factor-alpha (TNFalpha) in combination with cycloheximide (CHX) on apoptosis in the human histiocytic lymphoma cell line U937. Cycloheximide 266-279 tumor necrosis factor Homo sapiens 207-234 25148872-1 2014 The present study is aimed to determine the protective effect of a novel nanoparticle with antioxidant properties, nanoceria, on reactive oxygen species (ROS) production, and calcium signaling evoked by the tumor necrosis factor-alpha (TNFalpha) in combination with cycloheximide (CHX) on apoptosis in the human histiocytic lymphoma cell line U937. Cycloheximide 266-279 tumor necrosis factor Homo sapiens 236-244 25148872-1 2014 The present study is aimed to determine the protective effect of a novel nanoparticle with antioxidant properties, nanoceria, on reactive oxygen species (ROS) production, and calcium signaling evoked by the tumor necrosis factor-alpha (TNFalpha) in combination with cycloheximide (CHX) on apoptosis in the human histiocytic lymphoma cell line U937. Cycloheximide 281-284 tumor necrosis factor Homo sapiens 207-234 25148872-1 2014 The present study is aimed to determine the protective effect of a novel nanoparticle with antioxidant properties, nanoceria, on reactive oxygen species (ROS) production, and calcium signaling evoked by the tumor necrosis factor-alpha (TNFalpha) in combination with cycloheximide (CHX) on apoptosis in the human histiocytic lymphoma cell line U937. Cycloheximide 281-284 tumor necrosis factor Homo sapiens 236-244 23397952-6 2013 Cells were treated with TNF-alpha alone or in the presence of cycloheximide (CHX), which promotes caspase-8 activation by eliminating the endogenous caspase-8 inhibitor, c-FLIP. Cycloheximide 77-80 tumor necrosis factor Homo sapiens 24-33 24466329-4 2014 Pretreatment with the protein synthesis inhibitor cycloheximide or the protein kinase C inhibitor calphostin C prior to the addition of TNF completely abrogated the TNF-induced increment in peak bradykinin response. Cycloheximide 50-63 tumor necrosis factor Homo sapiens 165-168 23751896-6 2013 RESULTS: TNF + CHX-induced death of Huh7 cells involved JNK activation since it was partially prevented by suppressing JNK activity or expression. Cycloheximide 15-18 tumor necrosis factor Homo sapiens 9-12 22977259-2 2012 FAM129B protein, which is a member of a small family of proteins, was also found to suppress TNFalpha/cycloheximide-induced apoptosis in HeLa cells. Cycloheximide 102-115 tumor necrosis factor Homo sapiens 93-101 22363611-1 2012 Although TNFalpha is a strong inducer of apoptosis, its cytotoxicity in most normal cells in vitro requires blockade of NFkappaB signaling or inhibition of de novo protein synthesis, typically by the addition of cycloheximide. Cycloheximide 212-225 tumor necrosis factor Homo sapiens 9-17 22534375-11 2012 Tumour necrosis factor-alpha (TNF-alpha) significantly increased GLS expression in RA FLSs; this effect was reduced by pre-treatment with cycloheximide and mithramycin. Cycloheximide 138-151 tumor necrosis factor Homo sapiens 30-39 22055894-10 2012 TWEAK induced RelB activation and suppressed IL-6 mRNA expression in TNFalpha-activated FLS and both of these phenomenon were abolished by inhibition of new protein synthesis with cycloheximide. Cycloheximide 180-193 tumor necrosis factor Homo sapiens 69-77 22660975-0 2012 Protective effect of Homer 1a on tumor necrosis factor-alpha with cycloheximide-induced apoptosis is mediated by mitogen-activated protein kinase pathways. Cycloheximide 66-79 tumor necrosis factor Homo sapiens 33-60 22660975-2 2012 In this study, we found that tumor necrosis factor-alpha (TNF-alpha)/cycloheximide (CHX) treatment transiently increased Homer 1a (the short variant of Homer 1), but did not affect Homer 1b/c (the long variant of Homer 1). Cycloheximide 69-82 tumor necrosis factor Homo sapiens 29-56 22660975-2 2012 In this study, we found that tumor necrosis factor-alpha (TNF-alpha)/cycloheximide (CHX) treatment transiently increased Homer 1a (the short variant of Homer 1), but did not affect Homer 1b/c (the long variant of Homer 1). Cycloheximide 84-87 tumor necrosis factor Homo sapiens 29-56 22555848-6 2012 Polyamine-deficient cells also exhibited an increase in resistance to tumor necrosis factor-alpha/cycloheximide-induced apoptosis, which was prevented by inhibiting SG formation with silencing SG resident proteins Sort1 and TIA-1. Cycloheximide 98-111 tumor necrosis factor Homo sapiens 70-97 22314197-6 2012 The presence of 2% PRP significantly inhibited serum starvation- or TNF-alpha/cycloheximide-induced apoptosis in comparison to 2% FBS or 2% PPP. Cycloheximide 78-91 tumor necrosis factor Homo sapiens 68-77 22301110-4 2012 Here, we show that long-term exposure of 18Co cells, a model of human colonic myofibroblasts, with TNF-alpha led to a striking increase in cell surface EGFR expression, an effect that was completely inhibited by cycloheximide. Cycloheximide 212-225 tumor necrosis factor Homo sapiens 99-108 22198289-2 2012 Stimulation of human umbilical vein endothelial cells (HUVEC) with IL-1beta or TNF-alpha/cycloheximide (CHX) was found to enhance the phosphorylation of p38 and Jun-N-terminal kinase (JNK) in a time-dependent fashion, but did not affect the time-dependent phosphorylation of extracellular signal-regulated kinase. Cycloheximide 89-102 tumor necrosis factor Homo sapiens 79-88 22198289-2 2012 Stimulation of human umbilical vein endothelial cells (HUVEC) with IL-1beta or TNF-alpha/cycloheximide (CHX) was found to enhance the phosphorylation of p38 and Jun-N-terminal kinase (JNK) in a time-dependent fashion, but did not affect the time-dependent phosphorylation of extracellular signal-regulated kinase. Cycloheximide 104-107 tumor necrosis factor Homo sapiens 79-88 21537832-3 2011 We previously reported that TNFalpha-induced DcR3 overexpression in rheumatoid synovial fibroblasts (RA-FLS) protects the cells from Fas-induced apoptosis and that DcR3 induces VLA-4 expression in THP-1 macrophages to inhibit cycloheximide-induced apoptosis. Cycloheximide 226-239 tumor necrosis factor Homo sapiens 28-36 22319556-5 2012 Inhibition of protein synthesis by cycloheximide revealed that poly I:C- or LPS-induced secreted TNF-alpha is synthesized de novo, not released from cellular stores. Cycloheximide 35-48 tumor necrosis factor Homo sapiens 97-106 21903942-1 2011 OBJECTIVE: Tumor necrosis factor-alpha (TNFalpha) may change from a stimulator of reversible activation of endothelial cells (ECs) to a killer when combined with cycloheximide (CHX). Cycloheximide 162-175 tumor necrosis factor Homo sapiens 11-38 21903942-1 2011 OBJECTIVE: Tumor necrosis factor-alpha (TNFalpha) may change from a stimulator of reversible activation of endothelial cells (ECs) to a killer when combined with cycloheximide (CHX). Cycloheximide 162-175 tumor necrosis factor Homo sapiens 40-48 21903942-1 2011 OBJECTIVE: Tumor necrosis factor-alpha (TNFalpha) may change from a stimulator of reversible activation of endothelial cells (ECs) to a killer when combined with cycloheximide (CHX). Cycloheximide 177-180 tumor necrosis factor Homo sapiens 11-38 21903942-1 2011 OBJECTIVE: Tumor necrosis factor-alpha (TNFalpha) may change from a stimulator of reversible activation of endothelial cells (ECs) to a killer when combined with cycloheximide (CHX). Cycloheximide 177-180 tumor necrosis factor Homo sapiens 40-48 18180277-5 2008 Apoptosis of PBMCs was studied by stimulation with TNFalpha in the presence of cycloheximide and annexin V staining. Cycloheximide 79-92 tumor necrosis factor Homo sapiens 51-59 21506109-5 2011 However it decreased cell death in C-28/I2 chondrocytes exposed to stimuli previously reported to promptly trigger apoptosis, that is, the cytokine tumor necrosis factor-alpha (TNF) plus cycloheximide (CHX) or the polyamine analogue N(1),N(11)-diethylnorspermine (DENSPM) plus CHX. Cycloheximide 202-205 tumor necrosis factor Homo sapiens 177-180 21506109-5 2011 However it decreased cell death in C-28/I2 chondrocytes exposed to stimuli previously reported to promptly trigger apoptosis, that is, the cytokine tumor necrosis factor-alpha (TNF) plus cycloheximide (CHX) or the polyamine analogue N(1),N(11)-diethylnorspermine (DENSPM) plus CHX. Cycloheximide 277-280 tumor necrosis factor Homo sapiens 177-180 21350193-2 2011 TNF-alpha requires inhibition of antiapoptotic protein synthesis by cycloheximide (CHX). Cycloheximide 68-81 tumor necrosis factor Homo sapiens 0-9 21148485-7 2011 However, when apoptosis was induced by exposure to TNFalpha/cycloheximide or other apoptotic signaling molecules, the onset of apoptosis was accelerated 3-4-fold when FAM129B was depleted. Cycloheximide 60-73 tumor necrosis factor Homo sapiens 51-59 18465786-1 2008 We were looking by a proteomic approach for new phospho-proteins involved during the early steps of the TNF + cycloheximide (CHX)-induced apoptosis-preceding mitochondrial membrane permeabilization-of endothelial cells (BAEC). Cycloheximide 110-123 tumor necrosis factor Homo sapiens 104-107 18465786-1 2008 We were looking by a proteomic approach for new phospho-proteins involved during the early steps of the TNF + cycloheximide (CHX)-induced apoptosis-preceding mitochondrial membrane permeabilization-of endothelial cells (BAEC). Cycloheximide 125-128 tumor necrosis factor Homo sapiens 104-107 18336852-9 2008 Moreover, pretreatment with actinomycin D and cycloheximide attenuated TNF-alpha-induced MMP-9 expression. Cycloheximide 46-59 tumor necrosis factor Homo sapiens 71-80 18289527-2 2008 It has been established that the protein synthesis inhibitor cycloheximide (CHX) sensitizes many types of cells to tumor necrosis factor (TNF)-alpha-induced apoptosis, mainly due to its ability to block de novo synthesis of cellular FLICE-inhibitory protein (c-FLIP). Cycloheximide 61-74 tumor necrosis factor Homo sapiens 115-148 18442799-2 2008 The protein synthesis inhibitor cycloheximide (CHX) and its structural derivative acetoxycycloheximide (Ac-CHX) have been recently shown to block the TNF-alpha-induced activation of NF-kappaB via ectodomain shedding of TNF receptor 1 (TNF-R1) in human lung carcinoma A549 cells. Cycloheximide 32-45 tumor necrosis factor Homo sapiens 150-159 18442799-2 2008 The protein synthesis inhibitor cycloheximide (CHX) and its structural derivative acetoxycycloheximide (Ac-CHX) have been recently shown to block the TNF-alpha-induced activation of NF-kappaB via ectodomain shedding of TNF receptor 1 (TNF-R1) in human lung carcinoma A549 cells. Cycloheximide 47-50 tumor necrosis factor Homo sapiens 150-159 18485876-1 2008 The inflammatory response of mammalian cells to TNF-alpha can be switched to apoptosis either by cotreatment with a protein synthesis inhibitor, cycloheximide, or Smac mimetic, a small molecule mimic of Smac/Diablo protein. Cycloheximide 145-158 tumor necrosis factor Homo sapiens 48-57 18218673-0 2008 TNF-alpha/cycloheximide-induced apoptosis in intestinal epithelial cells requires Rac1-regulated reactive oxygen species. Cycloheximide 10-23 tumor necrosis factor Homo sapiens 0-9 18218673-1 2008 Previously we have shown that both Rac1 and c-Jun NH(2)-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-alpha/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive oxygen species (ROS) in apoptosis is unclear. Cycloheximide 149-162 tumor necrosis factor Homo sapiens 138-148 18218673-1 2008 Previously we have shown that both Rac1 and c-Jun NH(2)-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-alpha/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive oxygen species (ROS) in apoptosis is unclear. Cycloheximide 164-167 tumor necrosis factor Homo sapiens 138-148 18289527-2 2008 It has been established that the protein synthesis inhibitor cycloheximide (CHX) sensitizes many types of cells to tumor necrosis factor (TNF)-alpha-induced apoptosis, mainly due to its ability to block de novo synthesis of cellular FLICE-inhibitory protein (c-FLIP). Cycloheximide 76-79 tumor necrosis factor Homo sapiens 115-148 18289527-3 2008 Nevertheless, we have surprisingly found that CHX, as well as its structural analogue acetoxycycloheximide (Ac-CHX), prevents TNF-alpha-mediated activation of NF-kappaB and caspase-8 in human lung carcinoma A549 cells. Cycloheximide 46-49 tumor necrosis factor Homo sapiens 126-135 18086809-6 2008 Cell viability assays indicated that the p38 mitogen-activated protein kinase (MAPK) inhibitors SB202190 and SB203580 and the general protein synthesis inhibitor cycloheximide inhibited both the LPS and TNF-alpha sensitization of HUVEC to Stx2, while all other inhibitors tested did not inhibit this sensitization. Cycloheximide 162-175 tumor necrosis factor Homo sapiens 203-212 18439101-6 2008 TNF-alpha-induced JNK phosphorylation was sustained in the presence of cycloheximide, which was accompanied by accelerated neutrophil apoptosis. Cycloheximide 71-84 tumor necrosis factor Homo sapiens 0-9 17584970-3 2007 The increase in TNF-alpha production was prevented by actinomycin D and cycloheximide, indicating transcriptional activation of TNF-alpha gene. Cycloheximide 72-85 tumor necrosis factor Homo sapiens 16-25 17584970-3 2007 The increase in TNF-alpha production was prevented by actinomycin D and cycloheximide, indicating transcriptional activation of TNF-alpha gene. Cycloheximide 72-85 tumor necrosis factor Homo sapiens 128-137 17671691-8 2007 Actinomycin D suppressed and cycloheximide augmented CXCL-8 mRNA which was induced by TNF-alpha or not. Cycloheximide 29-42 tumor necrosis factor Homo sapiens 86-95 16985255-4 2007 In this study, we demonstrate that TNF-alpha treatment, in the presence of cycloheximide, also results in the rapid turnover of STAT5A and STAT5B in a process that is independent of STAT5 activation by tyrosine phosphorylation. Cycloheximide 75-88 tumor necrosis factor Homo sapiens 35-44 17435549-4 2007 Exposure of normal intestinal epithelial cells (IEC-6) to the conjugated bile salts taurodeoxycholate (TDCA) and taurochenodeoxycholate (TCDCA) resulted in an increase in resistance to tumor necrosis factor (TNF)-alpha and cycloheximide (CHX)-induced apoptosis, and NF-kappaB activation. Cycloheximide 223-236 tumor necrosis factor Homo sapiens 185-218 17435549-4 2007 Exposure of normal intestinal epithelial cells (IEC-6) to the conjugated bile salts taurodeoxycholate (TDCA) and taurochenodeoxycholate (TCDCA) resulted in an increase in resistance to tumor necrosis factor (TNF)-alpha and cycloheximide (CHX)-induced apoptosis, and NF-kappaB activation. Cycloheximide 238-241 tumor necrosis factor Homo sapiens 185-218 16985255-6 2007 Initial characterization of the TNF-alpha and cycloheximide-mediated degradation of STAT5 indicates that inhibition of the proteasome stabilizes both forms of STAT5 in the presence of TNF-alpha. Cycloheximide 46-59 tumor necrosis factor Homo sapiens 184-193 16077198-3 2005 Nonetheless, co-incubation TNF-alpha (10 ng/ml) with cycloheximide (5 micro g/ml, CHX) caused time-dependent (6, 12, 24 hours) cell death even though, at that concentration cycloheximide did not exert cytotoxic effect unless 24 hour of treatment. Cycloheximide 53-66 tumor necrosis factor Homo sapiens 27-36 17069807-2 2006 Using ECV304 cells, which can be made TNFalpha-sensitive by cycloheximide (CHX) co-treatment, we evaluated the potential roles of ceramide and phospholipase D (PLD) in TNFalpha-induced apoptosis. Cycloheximide 60-73 tumor necrosis factor Homo sapiens 38-46 17069807-2 2006 Using ECV304 cells, which can be made TNFalpha-sensitive by cycloheximide (CHX) co-treatment, we evaluated the potential roles of ceramide and phospholipase D (PLD) in TNFalpha-induced apoptosis. Cycloheximide 75-78 tumor necrosis factor Homo sapiens 38-46 16339571-9 2005 Pretreatment with either actinomycin D or cycloheximide abolished TNF-alpha-induced PTX3 expression, indicating the requirement for both transcriptional and translational regulation. Cycloheximide 42-55 tumor necrosis factor Homo sapiens 66-75 16931628-3 2006 To overcome this problem in vitro, specific NF-kappaB inhibitors or transcription or protein synthesis inhibitors such as actinomycin D and cycloheximide are usually used in combination to increase TNFalpha killing of tumor cells. Cycloheximide 140-153 tumor necrosis factor Homo sapiens 198-206 16479515-7 2006 CXCL-8 mRNA was superinduced by TNF- alpha in the presence of the protein-synthesis inhibitor cycloheximide. Cycloheximide 94-107 tumor necrosis factor Homo sapiens 32-42 16330024-7 2006 Stimulation with TNF-alpha protected each cell type from apoptosis induced by TNF-alpha and cycloheximide. Cycloheximide 92-105 tumor necrosis factor Homo sapiens 17-26 15913957-5 2005 Treatment of NESK-transfected HeLa cells with TNF-alpha in the presence of cycloheximide or with staurosporine induced proteolytic cleavage of NESK. Cycloheximide 75-88 tumor necrosis factor Homo sapiens 46-55 16077198-0 2005 Cycloheximide-mediated sensitization to TNF-alpha-induced apoptosis in human colorectal cancer cell line COLO 205; role of FLIP and metabolic inhibitors. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 40-49 16077198-3 2005 Nonetheless, co-incubation TNF-alpha (10 ng/ml) with cycloheximide (5 micro g/ml, CHX) caused time-dependent (6, 12, 24 hours) cell death even though, at that concentration cycloheximide did not exert cytotoxic effect unless 24 hour of treatment. Cycloheximide 173-186 tumor necrosis factor Homo sapiens 27-36 16077198-6 2005 PKCs inhibitor staurosporine (5 microM) did not influence, whereas cPKC activator PMA (100 microM) prevented TNF-alpha-induced apoptosis in the presence of CHX. Cycloheximide 156-159 tumor necrosis factor Homo sapiens 109-118 16077199-0 2005 Position of STAT-1 alpha in cycloheximide-dependent apoptosis triggered by TNF-alpha in human colorectal COLO 205 cancer cell line; role of polyphenolic compounds. Cycloheximide 28-41 tumor necrosis factor Homo sapiens 75-84 16077199-6 2005 However, when TNF-alpha (10 ng/ml) has been given along with cycloheximide (5 micro g/ml, CHX) COLO 205 cells died extensively from apoptosis. Cycloheximide 61-74 tumor necrosis factor Homo sapiens 14-23 16077199-7 2005 Apparently, cycloheximide sensitized cells to TNF-alpha-induced programmed cell death. Cycloheximide 12-25 tumor necrosis factor Homo sapiens 46-55 15459750-8 2004 Additionally, coincubation with cycloheximide blocked the mitotic effects of GM-CSF or IL-3, allowing only the apoptotic responses of TNF to persist. Cycloheximide 32-45 tumor necrosis factor Homo sapiens 134-137 15701621-6 2005 The TNF-alpha increase in MLCK protein expression paralleled the increase in Caco-2 TJ permeability, and the inhibition of the TNF-alpha-induced MLCK expression (by cycloheximide) prevented the increase in Caco-2 TJ permeability, suggesting that MLCK expression may be required for the increase in Caco-2 TJ permeability. Cycloheximide 165-178 tumor necrosis factor Homo sapiens 127-136 15701621-10 2005 The cycloheximide inhibition of MLCK protein expression prevented the TNF-alpha increase in MLCK activity and Caco-2 TJ permeability. Cycloheximide 4-17 tumor necrosis factor Homo sapiens 70-79 15358608-10 2005 Cycloheximide, an inhibitor of protein synthesis, enhanced the toxicity of TNF in Ep-SMCs. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 75-78 15659777-4 2004 We demonstrate that exogenous, recombinant, TIMP-1 efficiently prevents apoptosis induced by TNFalpha in cycloheximide-sensitized ECs. Cycloheximide 105-118 tumor necrosis factor Homo sapiens 93-101 15231489-4 2004 However, cycloheximide treatment prolonged the TNF-alpha-induced JNK-1 kinase activity beyond 60 min, suggesting that protein synthesis is required to limit this signaling cascade. Cycloheximide 9-22 tumor necrosis factor Homo sapiens 47-56 12869656-6 2003 In contrast, cells treated with tumor necrosis factor alpha plus cycloheximide (TNFalpha + CHX) first appeared in the early apoptotic fraction and then accumulated in the necrotic/late apoptotic fraction. Cycloheximide 65-78 tumor necrosis factor Homo sapiens 80-88 15266023-3 2004 Using flow cytometry analyses, TNFalpha enhanced CD38 expression in a manner that was time-(0-24 h), concentration-(0.1-40 ng/ml), and protein synthesis-(cycloheximide blockade) dependent. Cycloheximide 154-167 tumor necrosis factor Homo sapiens 31-39 15024023-6 2004 This activated Akt was associated with both decreased levels of active caspase-3 and increased resistance to tumor necrosis factor-alpha/cycloheximide-induced apoptosis. Cycloheximide 137-150 tumor necrosis factor Homo sapiens 109-136 12869656-7 2003 Both C2-ceramide and TNFalpha + CHX increased caspase 8- and 3-like activities in cytosolic extracts; however, treatment of cells with the broad-spectrum caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone protected NB16 cells from TNFalpha + CHX-induced cell death but did not prevent C2-ceramide cytotoxicity. Cycloheximide 32-35 tumor necrosis factor Homo sapiens 21-29 12869656-7 2003 Both C2-ceramide and TNFalpha + CHX increased caspase 8- and 3-like activities in cytosolic extracts; however, treatment of cells with the broad-spectrum caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone protected NB16 cells from TNFalpha + CHX-induced cell death but did not prevent C2-ceramide cytotoxicity. Cycloheximide 32-35 tumor necrosis factor Homo sapiens 249-257 12869656-7 2003 Both C2-ceramide and TNFalpha + CHX increased caspase 8- and 3-like activities in cytosolic extracts; however, treatment of cells with the broad-spectrum caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone protected NB16 cells from TNFalpha + CHX-induced cell death but did not prevent C2-ceramide cytotoxicity. Cycloheximide 260-263 tumor necrosis factor Homo sapiens 21-29 12663669-1 2003 In the presence of cycloheximide, tumor necrosis factor or interleukin-1 initiates caspase activation, loss of mitochondrial membrane potential (DeltaPsi), DNA degradation, and nuclear condensation and fragmentation characteristic of apoptotic cell death in human vascular endothelial cells (EC). Cycloheximide 19-32 tumor necrosis factor Homo sapiens 34-55 12694807-3 2003 Stimulation of neutrophils by TNF-alpha increased the levels of HSP27 in the presence, but not in the absence, of cycloheximide. Cycloheximide 114-127 tumor necrosis factor Homo sapiens 30-39 12808024-6 2003 Experiments with actinomycin D and cycloheximide also pointed to a transcriptional and translational process in facilitating the TNF-alpha response. Cycloheximide 35-48 tumor necrosis factor Homo sapiens 129-138 12694807-4 2003 Reverse transcription-polymerase chain reaction (RT-PCR) experiments showed that TNF-alpha also induced HSP27 mRNA in the presence of cycloheximide. Cycloheximide 134-147 tumor necrosis factor Homo sapiens 81-90 12393619-4 2003 We report here that broad-spectrum caspase inhibitors effectively attenuated apoptosis induced in human neutrophils by incubation with agonistic anti-Fas antibody or by coincubation with tumor necrosis factor-alpha (TNF-alpha) and cycloheximide ex vivo. Cycloheximide 231-244 tumor necrosis factor Homo sapiens 216-225 11813164-5 2002 In addition, cycloheximide similarly renders TNF-alpha pro-apoptotic, suggesting that NF-kappaB activation controls the production of a protein(s) that protects eosinophils from the cytotoxic effects of TNF-alpha. Cycloheximide 13-26 tumor necrosis factor Homo sapiens 45-54 12137744-5 2002 The inhibitors SB203580, PD98059, SN50, cycloheximide and D-ribofuranosylbenzimidazole each reduced the basal and TNFalpha-stimulated secretion of IL-1beta and also reduced IL-6 secretion with the exception of SN50. Cycloheximide 40-53 tumor necrosis factor Homo sapiens 114-122 12080469-5 2002 However, in combination with tumor necrosis factor-alpha (TNF-alpha), cycloheximide efficiently increases steady-state levels of c-myc, suggesting that selective stress conditions are required to increase c-myc protein stability. Cycloheximide 70-83 tumor necrosis factor Homo sapiens 58-67 12209935-6 2002 Comparative studies with neutrophils adherent under static conditions demonstrated time-dependent activation of caspases in TNF-alpha/cycloheximide-induced apoptosis, for which caspase-3 also was implicated. Cycloheximide 134-147 tumor necrosis factor Homo sapiens 124-133 12055072-8 2002 Cycloheximide blocked TNF-alpha-mediated antiapoptotic signaling, suggesting protein synthesis is required. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 22-31 11813164-5 2002 In addition, cycloheximide similarly renders TNF-alpha pro-apoptotic, suggesting that NF-kappaB activation controls the production of a protein(s) that protects eosinophils from the cytotoxic effects of TNF-alpha. Cycloheximide 13-26 tumor necrosis factor Homo sapiens 203-212 11849390-7 2002 RESULTS: TNF-alpha with cycloheximide for three hours caused apoptosis in 87% PMN compared to 2% in untreated controls (N=18; P < 0.01). Cycloheximide 24-37 tumor necrosis factor Homo sapiens 9-18 11849390-11 2002 Blocking caspase-3 activity prevented apoptosis in TNF-alpha with cycloheximide-treated cells (83% to 2%) and prevented compromised respiratory burst in response to ANCA. Cycloheximide 66-79 tumor necrosis factor Homo sapiens 51-60 11502212-0 2001 Focal adhesion kinase affects the sensitivity of human hepatocellular carcinoma cell line SMMC-7721 to tumor necrosis factor-alpha/cycloheximide-induced apoptosis by regulating protein kinase B levels. Cycloheximide 131-144 tumor necrosis factor Homo sapiens 103-130 11835405-7 2002 Irrespective of STAT1 status, TNF induced cytotoxic effects in the presence of cycloheximide (CHX) in both cell types. Cycloheximide 79-92 tumor necrosis factor Homo sapiens 30-33 11835405-7 2002 Irrespective of STAT1 status, TNF induced cytotoxic effects in the presence of cycloheximide (CHX) in both cell types. Cycloheximide 94-97 tumor necrosis factor Homo sapiens 30-33 11682609-3 2001 As shown in this study, apoptosis in human-derived HL-60 and U937 cells induced by treatment with actinomycin D or TNF-alpha in combination with cycloheximide, respectively, was indeed dose-dependently downregulated by prior infection with T. gondii, as determined by DNA fragmentation assays. Cycloheximide 145-158 tumor necrosis factor Homo sapiens 115-124 11502212-1 2001 Most cell lines are resistant to tumor necrosis factor-alpha (TNF-alpha) cytotoxicity and require cotreatment of TNF-alpha with cycloheximide (Chx) to undergo apoptosis. Cycloheximide 143-146 tumor necrosis factor Homo sapiens 113-122 11359904-6 2001 SV80 cells normally show resistance to TNF-related apoptosis-inducing ligand (TRAIL) and TNF, as apoptosis can be induced only in the presence of low concentrations of cycloheximide (CHX). Cycloheximide 168-181 tumor necrosis factor Homo sapiens 39-42 11463813-5 2001 Resistance to either FasL- or TNF-induced apoptosis is overcome when cells are incubated in the presence of the protein synthesis inhibitor cycloheximide. Cycloheximide 140-153 tumor necrosis factor Homo sapiens 30-33 11309811-4 2001 METHODS: Apoptosis of human MCF-7, U-937, or HL-60 cells was induced by camptothecin (CPT) or tumor necrosis factor-alpha (TNF-alpha) combined with cycloheximide (CHX). Cycloheximide 163-166 tumor necrosis factor Homo sapiens 123-132 11292320-4 2001 The U937(M) cells, however, were sensitive to the cytotoxic action of TNF both in the presence and absence of cycloheximide. Cycloheximide 110-123 tumor necrosis factor Homo sapiens 70-73 11245595-1 2001 In a previous study, it was found that exposure to tumor necrosis factor-alpha (TNF-alpha) potentiated the electrophysiological response to carbachol in a time-dependent and cycloheximide-sensitive manner. Cycloheximide 174-187 tumor necrosis factor Homo sapiens 51-78 11245595-1 2001 In a previous study, it was found that exposure to tumor necrosis factor-alpha (TNF-alpha) potentiated the electrophysiological response to carbachol in a time-dependent and cycloheximide-sensitive manner. Cycloheximide 174-187 tumor necrosis factor Homo sapiens 80-89 11399512-7 2001 Evidence in support of this notion includes (1) TNF-induced apoptosis only in A375-R8, but not A375-6 cells; (2) cycloheximide enabled TNF to induce apoptosis even in A375-6 cells; and (3) somatic hybrid cells between A375-6 and A375-R8 cells are resistant to TNF-induced apoptosis. Cycloheximide 113-126 tumor necrosis factor Homo sapiens 135-138 11399512-7 2001 Evidence in support of this notion includes (1) TNF-induced apoptosis only in A375-R8, but not A375-6 cells; (2) cycloheximide enabled TNF to induce apoptosis even in A375-6 cells; and (3) somatic hybrid cells between A375-6 and A375-R8 cells are resistant to TNF-induced apoptosis. Cycloheximide 113-126 tumor necrosis factor Homo sapiens 135-138 11162606-1 2001 While MCF-7 and BT-20 cells were responsive to TNF without any metabolic inhibitors, CAMA-1 and SKBR-3 cells responded to TNF in the presence of cycloheximide; MDA-MB-231 and Hs578t cells were resistant to TNF even in the presence of cycloheximide. Cycloheximide 145-158 tumor necrosis factor Homo sapiens 122-125 11226410-2 2001 We have found that treatment of A431 cells with tumor necrosis factor-alpha in the presence of cycloheximide resulted in the cleavage of epidermal growth factor receptor (EGFR) as well as the activation of caspase-3. Cycloheximide 95-108 tumor necrosis factor Homo sapiens 48-75 11162606-1 2001 While MCF-7 and BT-20 cells were responsive to TNF without any metabolic inhibitors, CAMA-1 and SKBR-3 cells responded to TNF in the presence of cycloheximide; MDA-MB-231 and Hs578t cells were resistant to TNF even in the presence of cycloheximide. Cycloheximide 145-158 tumor necrosis factor Homo sapiens 122-125 11162606-1 2001 While MCF-7 and BT-20 cells were responsive to TNF without any metabolic inhibitors, CAMA-1 and SKBR-3 cells responded to TNF in the presence of cycloheximide; MDA-MB-231 and Hs578t cells were resistant to TNF even in the presence of cycloheximide. Cycloheximide 234-247 tumor necrosis factor Homo sapiens 122-125 11162606-1 2001 While MCF-7 and BT-20 cells were responsive to TNF without any metabolic inhibitors, CAMA-1 and SKBR-3 cells responded to TNF in the presence of cycloheximide; MDA-MB-231 and Hs578t cells were resistant to TNF even in the presence of cycloheximide. Cycloheximide 234-247 tumor necrosis factor Homo sapiens 122-125 11162606-2 2001 Bisindolylmaleimide (BIM), an inhibitor of PKC, either alone (MCF-7 and BT-20) or in combination with cycloheximide enhanced sensitivity of these cells to TNF. Cycloheximide 102-115 tumor necrosis factor Homo sapiens 155-158 11299730-3 2001 Co-treatment of these cells with actinomycin D or cycloheximide enhances TNF-alpha induced apoptosis, suggesting that some TNF-alpha-derived signals can augment apoptosis. Cycloheximide 50-63 tumor necrosis factor Homo sapiens 73-82 11299730-3 2001 Co-treatment of these cells with actinomycin D or cycloheximide enhances TNF-alpha induced apoptosis, suggesting that some TNF-alpha-derived signals can augment apoptosis. Cycloheximide 50-63 tumor necrosis factor Homo sapiens 123-132 11748914-2 2001 The effect of TNF-alpha-induced apoptosis was exacerbated by the hypoxanthine-xanthine oxidase (HX/XO) system and cycloheximide (CHX), but alleviated by superoxide dismutase (SOD), suggesting that TNF-alpha-induced apoptosis may be due to oxidative stress, and independent of protein synthesis. Cycloheximide 114-127 tumor necrosis factor Homo sapiens 14-23 11748914-2 2001 The effect of TNF-alpha-induced apoptosis was exacerbated by the hypoxanthine-xanthine oxidase (HX/XO) system and cycloheximide (CHX), but alleviated by superoxide dismutase (SOD), suggesting that TNF-alpha-induced apoptosis may be due to oxidative stress, and independent of protein synthesis. Cycloheximide 129-132 tumor necrosis factor Homo sapiens 14-23 12053189-7 2001 When FAK was 60% reduced as a result of the transfection of SMMC-7721 cells with FAK antisense construct, the percentage of TNF-alpha/cycloheximide-induced apoptosis was enhanced at lower dose of TNF-alpha but decreased at higher dose of TNF-alpha, compared with the control. Cycloheximide 134-147 tumor necrosis factor Homo sapiens 124-133 12053189-7 2001 When FAK was 60% reduced as a result of the transfection of SMMC-7721 cells with FAK antisense construct, the percentage of TNF-alpha/cycloheximide-induced apoptosis was enhanced at lower dose of TNF-alpha but decreased at higher dose of TNF-alpha, compared with the control. Cycloheximide 134-147 tumor necrosis factor Homo sapiens 196-205 12053189-7 2001 When FAK was 60% reduced as a result of the transfection of SMMC-7721 cells with FAK antisense construct, the percentage of TNF-alpha/cycloheximide-induced apoptosis was enhanced at lower dose of TNF-alpha but decreased at higher dose of TNF-alpha, compared with the control. Cycloheximide 134-147 tumor necrosis factor Homo sapiens 196-205 12053189-9 2001 Therefore, FAK regulated TNF-alpha/cycloheximide-induced apoptosis in a biphase manner. Cycloheximide 35-48 tumor necrosis factor Homo sapiens 25-34 11077046-3 2000 Here we report that these cells can be rendered sensitive to TNFalpha killing by treatment with the translational inhibitor cycloheximide, suggesting the existence of proteins that can suppress the death stimulus induced by the cytokine. Cycloheximide 124-137 tumor necrosis factor Homo sapiens 61-69 11131645-6 2000 Furthermore, our data explained why application of low concentrations of cycloheximide can sensitize cells for apoptosis induction by TNF-alpha. Cycloheximide 73-86 tumor necrosis factor Homo sapiens 134-143 11068016-3 2000 After pretreatment of neutrophils with cycloheximide or actinomycin D, TNF-alpha produced morphologically typical apoptosis in a time- and concentration-dependent manner. Cycloheximide 39-52 tumor necrosis factor Homo sapiens 71-80 11068016-5 2000 Caspase-3 activation by TNF-alpha was significantly enhanced by pretreatment with both cycloheximide and pyrrolidine dithiocarbamate. Cycloheximide 87-100 tumor necrosis factor Homo sapiens 24-33 11097743-4 2000 Further experiments suggested that cycloheximide (CHX), a protein synthesis inhibitor, increased the levels of p21(WAF1)mRNA and the induction of p21(WAF1)mRNA by TNF-alpha did not require new protein synthesis. Cycloheximide 35-48 tumor necrosis factor Homo sapiens 163-172 11097743-4 2000 Further experiments suggested that cycloheximide (CHX), a protein synthesis inhibitor, increased the levels of p21(WAF1)mRNA and the induction of p21(WAF1)mRNA by TNF-alpha did not require new protein synthesis. Cycloheximide 50-53 tumor necrosis factor Homo sapiens 163-172 11032726-2 2000 We have found that E-73, an acetoxyl analogue of cycloheximide, specifically blocks TNF-induced ICAM-1 expression even at concentrations unable to affect protein synthesis. Cycloheximide 49-62 tumor necrosis factor Homo sapiens 84-87 11032726-3 2000 By contrast, cycloheximide inhibited both TNF- and IL-1-induced ICAM-1 expression primarily due to the blockage of protein synthesis. Cycloheximide 13-26 tumor necrosis factor Homo sapiens 42-45 11018481-6 2000 Even greater effects on specificity of PtdSer synthesis, movement to CFMV and inhibition by z-VAD-fmk were observed in apoptotic cells induced by UV irradiation or tumor necrosis factor-alpha/cycloheximide treatment. Cycloheximide 192-205 tumor necrosis factor Homo sapiens 164-191 10942603-5 2000 Apoptosis of HL-60 cells was induced by DNA topoisomerase I inhibitor camptothecin (CPT) or tumor necrosis factor-alpha combined with cycloheximide (TNF-alpha + CHX). Cycloheximide 134-147 tumor necrosis factor Homo sapiens 149-158 10947155-5 2000 Cycloheximide (10 microM) prevented the transcriptional down-regulation of Cox-2 mRNA and to a lesser extent, TNFalpha mRNA, in LPS-tolerant cells. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 110-118 10926555-6 2000 Inhibition of new protein synthesis by cycloheximide blocked the increase in Galpha(i-2) protein induced by TNF-alpha. Cycloheximide 39-52 tumor necrosis factor Homo sapiens 108-117 10873159-7 2000 Release of IL-6 elicited by TNF-alpha was significantly inhibited by dexamethasone, cycloheximide, and nordihydroguaiaretic acid (NDGA). Cycloheximide 84-97 tumor necrosis factor Homo sapiens 28-37 10947155-10 2000 However, cycloheximide augmented both Cox-2 and TNFalpha mRNA expression in this group. Cycloheximide 9-22 tumor necrosis factor Homo sapiens 48-56 10653982-3 2000 We show that increased activity of several metalloproteases on the HeLa cell surface occurs after stresses due to UVC, actinomycin D, cycloheximide, and cisplatinum, which induce the release of transforming growth factor-alpha (TGFalpha) and other bioactive molecules. Cycloheximide 134-147 tumor necrosis factor Homo sapiens 194-226 10873576-3 2000 TNF-alpha-resistant NCI-H157 cells became sensitized to TNF-alpha by prior treatment with cycloheximide, suggesting the presence of newly synthesized antiapoptotic protein(s). Cycloheximide 90-103 tumor necrosis factor Homo sapiens 0-9 10873576-3 2000 TNF-alpha-resistant NCI-H157 cells became sensitized to TNF-alpha by prior treatment with cycloheximide, suggesting the presence of newly synthesized antiapoptotic protein(s). Cycloheximide 90-103 tumor necrosis factor Homo sapiens 56-65 10537278-3 1999 Forced expression of the dominant negative HOSdeltaF construct inhibited IkappaB degradation and led to sensitization of melanoma cells to apoptosis induced by tumor necrosis factor alpha with cycloheximide, as well as by cisplatin and ionizing and UV irradiation. Cycloheximide 193-206 tumor necrosis factor Homo sapiens 160-187 10620119-10 2000 Tumor necrosis factor-alpha induced production of C3 and interferon-gamma induced production of factor B were inhibited by cycloheximide. Cycloheximide 123-136 tumor necrosis factor Homo sapiens 0-27 10616218-12 1999 TNF-alpha sensitivity and NO2 production were completely restored by the addition of CX. Cycloheximide 85-87 tumor necrosis factor Homo sapiens 0-9 10484519-5 1999 Moreover, a posttranscriptional mechanism(s) appears to contribute significantly to COX-2 mRNA accumulation as pretreatment for 15 min with cycloheximide (CHX, 1 microM) caused a superinduction of COX-2 mRNA accumulation in unstimulated cells as well as in cells challenged with either TNF or PMA. Cycloheximide 140-153 tumor necrosis factor Homo sapiens 286-289 10484519-5 1999 Moreover, a posttranscriptional mechanism(s) appears to contribute significantly to COX-2 mRNA accumulation as pretreatment for 15 min with cycloheximide (CHX, 1 microM) caused a superinduction of COX-2 mRNA accumulation in unstimulated cells as well as in cells challenged with either TNF or PMA. Cycloheximide 155-158 tumor necrosis factor Homo sapiens 286-289 10364265-6 1999 In parallel, transmembrane TNF-expressing HeLa cells display high sensitivity to cycloheximide or interferon-gamma, similar to untransfected cells treated with these agents in combination with sTNF. Cycloheximide 81-94 tumor necrosis factor Homo sapiens 27-30 10393506-11 1999 Cycloheximide prevented the binding activity of the cytosolic protein to 3"-UTR eNOS mRNA related to TNF-alpha; this effect was associated with greater eNOS mRNA levels. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 101-110 10470105-6 1999 Incubation with TNF alpha (+/- cycloheximide) led to activation of the caspase cascade and was followed by apoptosis. Cycloheximide 31-44 tumor necrosis factor Homo sapiens 16-25 10222064-5 1999 Cycloheximide (protein synthesis inhibitor), tunicamycin (N-linked glycosylation inhibitor), and beta-d-xyloside (chondroitin sulfation inhibitor) all inhibited IL-4-mediated downregulation of TNFalpha-induced monocyte HA binding. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 193-201 10360689-19 1999 Blocking RNA synthesis with actinomycin D or preventing protein synthesis with cycloheximide abolished or decreased particle-induced release of TNF-alpha and IL-6 from the macrophages. Cycloheximide 79-92 tumor necrosis factor Homo sapiens 144-153 10393506-7 1999 In addition, TNF-alpha reduced eNOS mRNA levels and this was prevented by coincubation with cycloheximide. Cycloheximide 92-105 tumor necrosis factor Homo sapiens 13-22 10364265-7 1999 Moreover, cycloheximide-induced apoptosis in transmembrane TNF transfectants can be blocked by the caspase inhibitor zVAD-fmk and does not necessarily need cell to cell contact, indicating a critical role of constitutive autotropic signaling of TNF.TNF receptor complexes. Cycloheximide 10-23 tumor necrosis factor Homo sapiens 59-62 10364265-7 1999 Moreover, cycloheximide-induced apoptosis in transmembrane TNF transfectants can be blocked by the caspase inhibitor zVAD-fmk and does not necessarily need cell to cell contact, indicating a critical role of constitutive autotropic signaling of TNF.TNF receptor complexes. Cycloheximide 10-23 tumor necrosis factor Homo sapiens 245-248 10364265-7 1999 Moreover, cycloheximide-induced apoptosis in transmembrane TNF transfectants can be blocked by the caspase inhibitor zVAD-fmk and does not necessarily need cell to cell contact, indicating a critical role of constitutive autotropic signaling of TNF.TNF receptor complexes. Cycloheximide 10-23 tumor necrosis factor Homo sapiens 245-248 9813034-1 1998 Most normal and neoplastic cell types are resistant to tumor necrosis factor (TNF) cytotoxicity unless cotreated with protein or RNA synthesis inhibitors, such as cycloheximide and actinomycin D. Cycloheximide 163-176 tumor necrosis factor Homo sapiens 55-76 10355595-1 1999 Treatment of neutrophils with tumor necrosis factor-alpha (TNF-alpha) in the presence of cycloheximide induced apoptosis within 3 h, as evaluated by the occurrence of morphological nuclear changes characteristic of apoptosis. Cycloheximide 89-102 tumor necrosis factor Homo sapiens 30-57 10355595-1 1999 Treatment of neutrophils with tumor necrosis factor-alpha (TNF-alpha) in the presence of cycloheximide induced apoptosis within 3 h, as evaluated by the occurrence of morphological nuclear changes characteristic of apoptosis. Cycloheximide 89-102 tumor necrosis factor Homo sapiens 59-68 10355595-2 1999 Pretreatment of neutrophils with dibutyryl cyclic AMP (dbcAMP) suppressed the TNF-alpha/cycloheximide-induced apoptosis in neutrophils in a concentration-dependent manner, while dbcAMP by itself did not induce any morphological changes. Cycloheximide 88-101 tumor necrosis factor Homo sapiens 78-87 10355595-5 1999 DbcAMP also inhibited the TNF-alpha/cycloheximide-induced activation of caspase-3, but it had no effect on the activation of caspase-8 in human neutrophils. Cycloheximide 36-49 tumor necrosis factor Homo sapiens 26-35 10201951-7 1999 Further, EMSA with human fibroblast nuclear extracts demonstrated enhanced binding of a single, specific complex within 5 min of TNF-alpha stimulation, which reached a plateau by 1 h and was not affected by preincubation of cells with cycloheximide. Cycloheximide 235-248 tumor necrosis factor Homo sapiens 129-138 10066786-1 1999 Cycloheximide (CHX) can contribute to apoptotic processes, either in conjunction with another agent (e.g. tumor necrosis factor-alpha) or on its own. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 106-133 10066786-1 1999 Cycloheximide (CHX) can contribute to apoptotic processes, either in conjunction with another agent (e.g. tumor necrosis factor-alpha) or on its own. Cycloheximide 15-18 tumor necrosis factor Homo sapiens 106-133 9933632-6 1999 Furthermore, cycloheximide displayed a similar capacity to enhance TNF-alpha induced neutrophil apoptosis even at time points when cycloheximide alone had no pro-apoptotic effect, suggesting that NF-kappaB may regulate the production of protein(s) which protect neutrophils from the cytotoxic effects of TNF-alpha. Cycloheximide 13-26 tumor necrosis factor Homo sapiens 67-76 9933632-6 1999 Furthermore, cycloheximide displayed a similar capacity to enhance TNF-alpha induced neutrophil apoptosis even at time points when cycloheximide alone had no pro-apoptotic effect, suggesting that NF-kappaB may regulate the production of protein(s) which protect neutrophils from the cytotoxic effects of TNF-alpha. Cycloheximide 13-26 tumor necrosis factor Homo sapiens 304-313 9917505-10 1999 In addition, the induction of MMP-9 expression by TNF-alpha was completely abrogated in the presence of cycloheximide, a protein synthesis inhibitor, suggesting that de novo protein synthesis may be required. Cycloheximide 104-117 tumor necrosis factor Homo sapiens 50-59 9813034-1 1998 Most normal and neoplastic cell types are resistant to tumor necrosis factor (TNF) cytotoxicity unless cotreated with protein or RNA synthesis inhibitors, such as cycloheximide and actinomycin D. Cycloheximide 163-176 tumor necrosis factor Homo sapiens 78-81 9686620-0 1998 Sustained phosphorylation of cytosolic phospholipase A2 accompanies cycloheximide- and adenovirus-induced susceptibility to TNF. Cycloheximide 68-81 tumor necrosis factor Homo sapiens 124-127 9713511-8 1998 It occurs mostly through type I (p55) TNF receptors, probably involves a calphostin-C sensitive protein kinase C activity and requires synthesis of proteins (it is inhibited by actinomycin D or cycloheximide) and of inducible nitric oxide (NO) synthase (it is inhibited by NG-methyl-L-arginine or aminoguanidine). Cycloheximide 194-207 tumor necrosis factor Homo sapiens 38-41 9533826-8 1998 Cycloheximide (9 micron), a protein synthesis inhibitor, decreased TNF-alpha-stimulated levels for ir-ET-1 and ir-Big ET-1, suggesting that TNF-alpha may be directly regulating ET-1 expression at the ET-1 gene. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 67-76 9637506-6 1998 The protein synthesis inhibitor, cycloheximide, increased TNF-induced cPLA2 activity and cytotoxicity in both CEM and CEM/VLB100 cell lines. Cycloheximide 33-46 tumor necrosis factor Homo sapiens 58-61 9769910-10 1998 However, TNF can cause apoptosis of EC when cells are co-treated with either the protein synthesis inhibitor cycloheximide (CHX) or the lipid mediator ceramide (cer). Cycloheximide 109-122 tumor necrosis factor Homo sapiens 9-12 9769910-10 1998 However, TNF can cause apoptosis of EC when cells are co-treated with either the protein synthesis inhibitor cycloheximide (CHX) or the lipid mediator ceramide (cer). Cycloheximide 124-127 tumor necrosis factor Homo sapiens 9-12 10200470-3 1998 We report here that rapid apoptosis induced by TNF in U937 cells or anti-Fas in Jurkat cells, in the presence of cycloheximide, induced only a very low increase (<20%) in the cell ceramide content. Cycloheximide 113-126 tumor necrosis factor Homo sapiens 47-50 9461593-6 1998 However, when the cells were pretreated with actinomycin D or cycloheximide, TNF-alpha stimulated a second sustained JNK activity peak. Cycloheximide 62-75 tumor necrosis factor Homo sapiens 77-86 9533826-8 1998 Cycloheximide (9 micron), a protein synthesis inhibitor, decreased TNF-alpha-stimulated levels for ir-ET-1 and ir-Big ET-1, suggesting that TNF-alpha may be directly regulating ET-1 expression at the ET-1 gene. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 140-149 9120022-5 1997 TNFalpha- and IL-1beta-induced increases in eotaxin mRNA were diminished in a dose-dependent manner by the glucocorticoid dexamethasone and were augmented by the protein synthesis inhibitor cycloheximide. Cycloheximide 190-203 tumor necrosis factor Homo sapiens 0-8 9344602-0 1997 Influence of cycloheximide-mediated downregulation of glucose transport on TNF alpha-induced apoptosis. Cycloheximide 13-26 tumor necrosis factor Homo sapiens 75-84 9344602-1 1997 Enhancement of cellular sensitivity to TNF alpha-induced apoptosis by cycloheximide (CX) has been attributed to its quality as an inhibitor of protein synthesis, presumably by prevention of the synthesis of short-lived death antagonists. Cycloheximide 70-83 tumor necrosis factor Homo sapiens 39-48 9344602-1 1997 Enhancement of cellular sensitivity to TNF alpha-induced apoptosis by cycloheximide (CX) has been attributed to its quality as an inhibitor of protein synthesis, presumably by prevention of the synthesis of short-lived death antagonists. Cycloheximide 85-87 tumor necrosis factor Homo sapiens 39-48 9344602-10 1997 In conclusion, CX is proposed to contribute to TNF alpha-induced apoptosis predominantly by interference with glucose transport; the exact nature of this effect remains to be elucidated. Cycloheximide 15-17 tumor necrosis factor Homo sapiens 47-56 9314949-2 1997 However, the combination of TNF and the protein synthesis inhibitor cycloheximide (CHX) induces apoptosis in up to 50% of EC within 24 hours. Cycloheximide 83-86 tumor necrosis factor Homo sapiens 28-31 9374730-8 1997 In addition, cycloheximide, a protein synthesis inhibitor, completely blocked the potentiating effect of TNF-alpha on Ca2+ signals. Cycloheximide 13-26 tumor necrosis factor Homo sapiens 105-114 9089293-6 1997 Cycloheximide strongly increased IL-1beta-induced TNF-alpha mRNA concentration indicating that de novo protein synthesis is not required for TNF-alpha gene expression. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 50-59 8631819-11 1996 Reduction in macrophage scavenger receptor message in response to TNF-alpha was dependent on new protein synthesis because it was blocked by cycloheximide. Cycloheximide 141-154 tumor necrosis factor Homo sapiens 66-75 8955085-10 1996 Cycloheximide abolished the TNF-alpha and IL-1beta effect, suggesting that de novo protein synthesis is required for receptor down-regulation. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 28-37 9014820-8 1996 Cycloheximide analysis demonstrated that protein synthesis may be required for TNF-alpha-mediated MT-MMP expression on synovial fibroblasts. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 79-88 8912727-7 1996 We have found that, when the HaCaT cells were sensitized by the translation inhibitor cycloheximide, TNF-alpha induced apoptosis, as evidenced by nuclear disintegration, DNA fragmentation ("DNA laddering"), and the appearance of soluble DNA/histone complexes. Cycloheximide 86-99 tumor necrosis factor Homo sapiens 101-110 8753710-7 1996 The production of TNF-alpha was inhibited in a dose-dependent manner by the translational inhibitor cycloheximide and the transcriptional inhibitor actinomycin D, indicating the requirement for both mRNA (messenger RNA) and protein synthesis for the induction of cytokine synthesis by titanium particles. Cycloheximide 100-113 tumor necrosis factor Homo sapiens 18-27 8695817-9 1996 The addition of TNF alpha to either cycloheximide or of actinomycin D-treated PMN overcame the inhibition, indicating that the effect was specific for TNF alpha. Cycloheximide 36-49 tumor necrosis factor Homo sapiens 16-25 8683130-1 1996 Previously we have shown that treatment of ML-1a cells with TNF in the presence of cycloheximide triggers apoptosis within 90 min. Cycloheximide 83-96 tumor necrosis factor Homo sapiens 60-63 9048649-6 1997 However, both E-selectin mRNA and gene transcription were dramatically induced by TNF-alpha in the same cells pretreated with the protein synthesis inhibitor cycloheximide. Cycloheximide 158-171 tumor necrosis factor Homo sapiens 82-91 9048649-9 1997 Cycloheximide pretreatment enabled immortalized human dermal microvascular endothelial cells that have lost the ability to express E-selectin to induce both E-selectin mRNA and gene transcription in response to TNF-alpha. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 211-220 9048649-10 1997 Induction of E-selectin mRNA by lipopolysaccharide or TNF-alpha in cycloheximide-treated HASMCs was inhibited by the antioxidant pyrrolidinedithiocarbamate and the serine protease inhibitor N alpha-L-tosyl-L-phenylalanine chloromethyl ketone, suggesting that a nuclear factor-kappa B-like mechanism may play an important role in E-selectin gene expression in HASMCs. Cycloheximide 67-80 tumor necrosis factor Homo sapiens 54-63 8993011-4 1997 Within 10 min of addition, TNF stimulated a significant increase in total cellular G alpha(i2), as determined by pertussis toxin-catalyzed ADP ribosylation, which was blocked by the translation inhibitor cycloheximide. Cycloheximide 204-217 tumor necrosis factor Homo sapiens 27-30 8993011-7 1997 Pretreatment with cycloheximide prevented the TNF-induced reduction in steady state alpha(i2) mRNA levels. Cycloheximide 18-31 tumor necrosis factor Homo sapiens 46-49 8892646-5 1996 We showed that apoptosis does occur in the monoblast/mononuclear phagocyte lineage, and that it could be induced in vitro by serum deprivation, UV light, or TNF-alpha in combination with cycloheximide (cx). Cycloheximide 202-204 tumor necrosis factor Homo sapiens 157-166 8804426-3 1996 Using the protein synthesis inhibitor cycloheximide and the antioxidant PDTC, that have an opposite effect on NF-kappa B and AP-1 activation, we showed that uPA mRNA induction by TNF-alpha and PMA in the A549 cell line is mainly due to NF-kappa B activation. Cycloheximide 38-51 tumor necrosis factor Homo sapiens 179-188 8774705-9 1996 Finally, when MCF-7 cells were treated with IL-1 beta or TNF-alpha in the presence of cycloheximide, transcription of IL-6 mRNA from the endogenous IL-6 gene was observed. Cycloheximide 86-99 tumor necrosis factor Homo sapiens 57-66 8613710-7 1996 Cycloheximide enhanced the IL-1 beta mRNA accumulation by GM-CSF at the level of mRNA stabilization, but blocked IL-1 beta mRNA expression by TNF. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 142-145 8867766-6 1996 The protein synthesis inhibitor cycloheximide abrogated the effects of IL-1 alpha, IL-1 beta and TNF-alpha on KGF gene induction, indicating that new protein synthesis is required in the process. Cycloheximide 32-45 tumor necrosis factor Homo sapiens 97-106 8709978-5 1996 Induction of Egr-1 mRNA by IL-1 beta and TNF-alpha was completely inhibited by H-7 suggesting the mediation of protein kinase C. The induction by IL-1 beta and TNF-alpha of Egr-1 mRNA was independent of de novo protein synthesis since this induction was also observed in the presence of protein synthesis inhibitor cycloheximide. Cycloheximide 315-328 tumor necrosis factor Homo sapiens 41-50 8709978-5 1996 Induction of Egr-1 mRNA by IL-1 beta and TNF-alpha was completely inhibited by H-7 suggesting the mediation of protein kinase C. The induction by IL-1 beta and TNF-alpha of Egr-1 mRNA was independent of de novo protein synthesis since this induction was also observed in the presence of protein synthesis inhibitor cycloheximide. Cycloheximide 315-328 tumor necrosis factor Homo sapiens 160-169 8697149-8 1996 Treatment of both cell types with anti-Fas led to time-dependent DNA fragmentation, but TNF-induced DNA fragmentation occurred only in the presence of cycloheximide. Cycloheximide 151-164 tumor necrosis factor Homo sapiens 88-91 8697149-7 1996 Interestingly, in the presence of cycloheximide, the kinetics of cell killing was more rapid for TNF than anti-Fas (50% inhibition occurred at 3 versus 6h). Cycloheximide 34-47 tumor necrosis factor Homo sapiens 97-100 8615653-5 1996 Cycloheximide superinduced the expression of TNF-alpha mRNA and, accordingly, the release of its protein. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 45-54 7579439-9 1995 Brief treatment of IL-1 alpha/TNF alpha-stimulated CDCL cells with cycloheximide before receptor induction reduces the synergistic increase in growth factor mRNA by 40% to 60% compared with cells not treated with CHX. Cycloheximide 67-80 tumor necrosis factor Homo sapiens 30-39 8598463-4 1996 Our experiments revealed a near perfect correlation between the activity of cPLA2 per cell and susceptibility to TNF in the presence of either cycloheximide (CHI) or actinomycin D (r = 0.97). Cycloheximide 143-156 tumor necrosis factor Homo sapiens 113-116 7579439-9 1995 Brief treatment of IL-1 alpha/TNF alpha-stimulated CDCL cells with cycloheximide before receptor induction reduces the synergistic increase in growth factor mRNA by 40% to 60% compared with cells not treated with CHX. Cycloheximide 213-216 tumor necrosis factor Homo sapiens 30-39 7664840-5 1995 Moreover, protein synthesis inhibitors such as cycloheximide (CHX) can facilitate apoptotic triggering by TNF, and mitochondrial function was suggested to be essential in the TNF-mediated apoptotic process. Cycloheximide 47-60 tumor necrosis factor Homo sapiens 106-109 7595061-5 1995 Cycloheximide treatment of the cultures containing M-CSF and IFN-gamma inhibited the production of IL-1 beta and TNF-alpha. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 113-122 7561073-2 1995 This cytotoxic effect does not involve the Fas death pathway and differs from the TNF-triggered death of tumor cells in several respects: 1) It is a slower process, requiring 2 to 3 days; 2) it is blocked, rather than enhanced, by cycloheximide; and 3) based on the agonistic effect of anti-TNF receptor Abs, it involves a synergistic effect of both the 55-kDa TNFR1 and the 75-kDa TNFR2, as opposed to the dominance of TNFR1 for tumor cytotoxicity. Cycloheximide 231-244 tumor necrosis factor Homo sapiens 82-85 7476903-3 1995 This effect was concentration dependent and resulted in a 20-40-fold increase in the release of TNF-alpha that was sensitive to actinomycin D and cycloheximide. Cycloheximide 146-159 tumor necrosis factor Homo sapiens 96-105 7662972-2 1995 Treatment of a human myelogenous leukemia cell line, ML-1a, with TNF in the presence of cycloheximide triggers endonucleolytic activity and apoptotic cell death within 90 minutes. Cycloheximide 88-101 tumor necrosis factor Homo sapiens 65-68 7664840-5 1995 Moreover, protein synthesis inhibitors such as cycloheximide (CHX) can facilitate apoptotic triggering by TNF, and mitochondrial function was suggested to be essential in the TNF-mediated apoptotic process. Cycloheximide 47-60 tumor necrosis factor Homo sapiens 175-178 7664840-5 1995 Moreover, protein synthesis inhibitors such as cycloheximide (CHX) can facilitate apoptotic triggering by TNF, and mitochondrial function was suggested to be essential in the TNF-mediated apoptotic process. Cycloheximide 62-65 tumor necrosis factor Homo sapiens 106-109 7664840-5 1995 Moreover, protein synthesis inhibitors such as cycloheximide (CHX) can facilitate apoptotic triggering by TNF, and mitochondrial function was suggested to be essential in the TNF-mediated apoptotic process. Cycloheximide 62-65 tumor necrosis factor Homo sapiens 175-178 7791344-5 1995 The TNF stimulatory effect was blocked by actinomycin D and cycloheximide. Cycloheximide 60-73 tumor necrosis factor Homo sapiens 4-7 7539458-5 1995 Forced expression of bcl-2 also attenuated TNF alpha-mediated cytotoxicity of glioma cell lines in the presence of actinomycin D and cycloheximide and conferred partial protection from irradiation and the cancer chemotherapy drugs, cisplatin and BCNU. Cycloheximide 133-146 tumor necrosis factor Homo sapiens 43-52 8531193-6 1995 However, the effect of TNF-alpha on P formation is blocked by cycloheximide (1 microgram/ml). Cycloheximide 62-75 tumor necrosis factor Homo sapiens 23-32 7640344-3 1995 The effects of TNF and IFN-beta were further distinguished by the action of the protein synthesis inhibitor cycloheximide, which reduced MT-II mRNA stimulation by TNF but enhanced IFN-beta-induced MT-II mRNA. Cycloheximide 108-121 tumor necrosis factor Homo sapiens 15-18 7640344-3 1995 The effects of TNF and IFN-beta were further distinguished by the action of the protein synthesis inhibitor cycloheximide, which reduced MT-II mRNA stimulation by TNF but enhanced IFN-beta-induced MT-II mRNA. Cycloheximide 108-121 tumor necrosis factor Homo sapiens 163-166 7895902-5 1994 The potentiating effect of 1,25(OH)2D3 on TNF action was abolished by cycloheximide indicating that their interaction requires protein synthesis. Cycloheximide 70-83 tumor necrosis factor Homo sapiens 42-45 7535734-5 1995 Similarly, TNF cytotoxicity occurred in Hep G2 cells sensitized with cycloheximide (CHX), and cytotoxicity to both inhibitors was dose dependent. Cycloheximide 69-82 tumor necrosis factor Homo sapiens 11-14 7535734-5 1995 Similarly, TNF cytotoxicity occurred in Hep G2 cells sensitized with cycloheximide (CHX), and cytotoxicity to both inhibitors was dose dependent. Cycloheximide 84-87 tumor necrosis factor Homo sapiens 11-14 7868906-9 1995 6) TNF-alpha-induced apoptosis of normal or inflammatory PBN and bone marrow neutrophils was enhanced by treatment with low doses of cycloheximide that alone were barely able to induce neutrophil apoptosis; however, apoptosis of PEN was not. Cycloheximide 133-146 tumor necrosis factor Homo sapiens 3-12 7989309-6 1994 In addition, by kinetically down-regulating TNF receptor expression with phorbol esters, cycloheximide, or trypsin, we determined that receptors were necessary for transduction of the TNF signal. Cycloheximide 89-102 tumor necrosis factor Homo sapiens 44-47 7989309-6 1994 In addition, by kinetically down-regulating TNF receptor expression with phorbol esters, cycloheximide, or trypsin, we determined that receptors were necessary for transduction of the TNF signal. Cycloheximide 89-102 tumor necrosis factor Homo sapiens 184-187 7836779-4 1995 The assay showed that TNF-dependent DNA fragmentation was potentiated by cycloheximide and occurred within 90 min. Cycloheximide 73-86 tumor necrosis factor Homo sapiens 22-25 7538424-8 1995 TNF-alpha-induced destabilization of cNOS mRNA could be partially prevented by coincubation with cycloheximide (1 mumol/L) but was not reproduced by addition of sodium nitroprusside. Cycloheximide 97-110 tumor necrosis factor Homo sapiens 0-9 8051422-11 1994 Furthermore, cycloheximide potentiated the TNF-mediated effect but not that mediated through anti-p60, thus also indicating a difference in the mechanism of action of these two agents. Cycloheximide 13-26 tumor necrosis factor Homo sapiens 43-46 7998962-11 1994 The constitutive NF-kappa B appears to be functionally active, since a low level of tumour necrosis factor (TNF) transcript is detectable in monocytes, and this level can be increased by blocking transcript degradation using cycloheximide. Cycloheximide 225-238 tumor necrosis factor Homo sapiens 84-106 7998962-11 1994 The constitutive NF-kappa B appears to be functionally active, since a low level of tumour necrosis factor (TNF) transcript is detectable in monocytes, and this level can be increased by blocking transcript degradation using cycloheximide. Cycloheximide 225-238 tumor necrosis factor Homo sapiens 108-111 7943343-4 1994 TNF-alpha-induced IL-8 mRNA expression showed a biphasic response in HAEC, with an early increase at 2 h followed by a sustained increase from 8 h, which was abolished by the addition of cycloheximide, suggesting that the synthesis of another protein was involved. Cycloheximide 187-200 tumor necrosis factor Homo sapiens 0-9 8204888-4 1994 Gelatinase induction by TNF-alpha and TPA was inhibited by actinomycin D or cycloheximide, indicating that de novo protein synthesis was required. Cycloheximide 76-89 tumor necrosis factor Homo sapiens 24-33 8065303-4 1994 On the other hand, there was a dramatic increase in c-Myc mRNA expression in TNF-alpha-sensitive D98 cells, but not in TNF-alpha-resistant H21 cells, which was only observed when the cells were treated with cycloheximide. Cycloheximide 207-220 tumor necrosis factor Homo sapiens 77-86 8063804-7 1994 The protein synthesis inhibitor cycloheximide inhibited collagenase mRNA induction by TNF or IFN-beta, suggesting that induction by both agents is indirect. Cycloheximide 32-45 tumor necrosis factor Homo sapiens 86-89 8151134-3 1993 When cycloheximide was added at the viral induction time, the inhibition of TNF-alpha superproduction and DNA synthesis was still observed. Cycloheximide 5-18 tumor necrosis factor Homo sapiens 76-85 8004813-4 1994 In contrast, IL-10 was weakly expressed when fibroblasts were stimulated with LPS, IL-1 alpha or tumour necrosis factor-alpha (TNF-alpha), but the expression was enhanced in the presence of cycloheximide combined with optimal concentrations of LPS, IL-1 alpha or TNF-alpha, IL-1 alpha was a more potent stimulator than LPS for GM-CSF, IL-6, IL-8 and IL-10 expression, but not for IL-1 alpha and IL-1 beta. Cycloheximide 190-203 tumor necrosis factor Homo sapiens 127-136 8004813-4 1994 In contrast, IL-10 was weakly expressed when fibroblasts were stimulated with LPS, IL-1 alpha or tumour necrosis factor-alpha (TNF-alpha), but the expression was enhanced in the presence of cycloheximide combined with optimal concentrations of LPS, IL-1 alpha or TNF-alpha, IL-1 alpha was a more potent stimulator than LPS for GM-CSF, IL-6, IL-8 and IL-10 expression, but not for IL-1 alpha and IL-1 beta. Cycloheximide 190-203 tumor necrosis factor Homo sapiens 263-272 8170983-3 1994 S-phase arrest also promoted tumor necrosis factor alpha-induced apoptosis, eliminating the normal requirement for simultaneous cycloheximide treatment. Cycloheximide 128-141 tumor necrosis factor Homo sapiens 29-56 7506700-4 1994 Cycloheximide, which abolished the cytokine-induced increase in nitrite production, had no effect on the interferon-gamma-induced increase in mRNA levels but partially inhibited that induced by interleukin-1 beta and markedly inhibited that induced by tumor necrosis factor-alpha. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 252-279 9419743-5 1994 RESULTS: The concentration-related stimulation of decidual PGE2 production by IL-1 beta and TNF alpha was completely abrogated by cycloheximide and actinomycin D treatment. Cycloheximide 130-143 tumor necrosis factor Homo sapiens 92-101 8014194-11 1994 Since inhibition of protein synthesis by cycloheximide also leads to a decrease in TNF receptors, it is possible that the density-dependent reduction in TNF receptor number is due to an overall decrease in protein synthesis. Cycloheximide 41-54 tumor necrosis factor Homo sapiens 83-86 8262257-4 1993 The results obtained indicate that the exposure of U937 cells to cycloheximide facilitates TNF-mediated PCD via a short term cell death program and modifies the expression of CD4 surface molecules. Cycloheximide 65-78 tumor necrosis factor Homo sapiens 91-94 8349628-11 1993 Pretreatment with cycloheximide prevented induction of LDL receptor mRNA by TNF, but not by IL-1, suggesting stimulation of LDL receptor transcription by TNF requires protein synthesis. Cycloheximide 18-31 tumor necrosis factor Homo sapiens 76-79 8311923-3 1993 RESULTS: Protein synthesis inhibition with cycloheximide or actinomycin D resulted in complete abrogation of the stimulation of PGE2 production by IL-1 beta, TNF alpha, and EGF. Cycloheximide 43-56 tumor necrosis factor Homo sapiens 158-167 8375478-8 1993 Coadministration of cycloheximide blocked the TNF-alpha-induced degradation of beta-actin mRNA. Cycloheximide 20-33 tumor necrosis factor Homo sapiens 46-55 8349628-11 1993 Pretreatment with cycloheximide prevented induction of LDL receptor mRNA by TNF, but not by IL-1, suggesting stimulation of LDL receptor transcription by TNF requires protein synthesis. Cycloheximide 18-31 tumor necrosis factor Homo sapiens 154-157 7683563-11 1993 Simultaneous addition of dexamethasone (0.01-1 microM) or cycloheximide (0.03-3 microM) inhibited in a concentration-dependent manner TNF alpha- and IL-1 beta-induced expression of Ca(2+)-independent NO synthase activity. Cycloheximide 58-71 tumor necrosis factor Homo sapiens 134-143 8250811-11 1993 Inhibition of protein synthesis by cycloheximide prevented the increase in VT receptors induced by TNF alpha. Cycloheximide 35-48 tumor necrosis factor Homo sapiens 99-108 8496597-0 1993 Differential action of cycloheximide and activation stimuli on transcription of tumor necrosis factor-alpha, IL-1 beta, IL-8, and P53 genes in human monocytes. Cycloheximide 23-36 tumor necrosis factor Homo sapiens 80-107 8496597-1 1993 In the present study we have analyzed superinduction of TNF-alpha mRNA and enhancement of TNF-alpha gene transcription by cycloheximide (Chx) in human blood monocytes isolated by continuous Percoll gradient and activated in vitro. Cycloheximide 122-135 tumor necrosis factor Homo sapiens 90-99 8496597-1 1993 In the present study we have analyzed superinduction of TNF-alpha mRNA and enhancement of TNF-alpha gene transcription by cycloheximide (Chx) in human blood monocytes isolated by continuous Percoll gradient and activated in vitro. Cycloheximide 137-140 tumor necrosis factor Homo sapiens 90-99 8483246-7 1993 In the presence of the protein synthesis inhibitor cycloheximide (CHX), the TNF mRNA level in the TNF resistant lines was increased while the sensitive lines required an additional signal, such as exogenous TNF, to upregulate the mRNA. Cycloheximide 51-64 tumor necrosis factor Homo sapiens 76-79 8483246-7 1993 In the presence of the protein synthesis inhibitor cycloheximide (CHX), the TNF mRNA level in the TNF resistant lines was increased while the sensitive lines required an additional signal, such as exogenous TNF, to upregulate the mRNA. Cycloheximide 51-64 tumor necrosis factor Homo sapiens 98-101 8483246-7 1993 In the presence of the protein synthesis inhibitor cycloheximide (CHX), the TNF mRNA level in the TNF resistant lines was increased while the sensitive lines required an additional signal, such as exogenous TNF, to upregulate the mRNA. Cycloheximide 51-64 tumor necrosis factor Homo sapiens 98-101 8483246-7 1993 In the presence of the protein synthesis inhibitor cycloheximide (CHX), the TNF mRNA level in the TNF resistant lines was increased while the sensitive lines required an additional signal, such as exogenous TNF, to upregulate the mRNA. Cycloheximide 66-69 tumor necrosis factor Homo sapiens 76-79 8483246-7 1993 In the presence of the protein synthesis inhibitor cycloheximide (CHX), the TNF mRNA level in the TNF resistant lines was increased while the sensitive lines required an additional signal, such as exogenous TNF, to upregulate the mRNA. Cycloheximide 66-69 tumor necrosis factor Homo sapiens 98-101 8483246-7 1993 In the presence of the protein synthesis inhibitor cycloheximide (CHX), the TNF mRNA level in the TNF resistant lines was increased while the sensitive lines required an additional signal, such as exogenous TNF, to upregulate the mRNA. Cycloheximide 66-69 tumor necrosis factor Homo sapiens 98-101 7685252-8 1993 This reduction in cNOS message in response to TNF-alpha depended on protein synthesis as it was blocked by cycloheximide. Cycloheximide 107-120 tumor necrosis factor Homo sapiens 46-55 8514874-2 1993 TNF-alpha protein was detectable by immunohistochemistry in blood eosinophils of hypereosinophilic subjects, and purified blood eosinophils from three atopic donors exhibited cycloheximide-inhibitable spontaneous release of TNF-alpha in vitro. Cycloheximide 175-188 tumor necrosis factor Homo sapiens 0-9 8514874-2 1993 TNF-alpha protein was detectable by immunohistochemistry in blood eosinophils of hypereosinophilic subjects, and purified blood eosinophils from three atopic donors exhibited cycloheximide-inhibitable spontaneous release of TNF-alpha in vitro. Cycloheximide 175-188 tumor necrosis factor Homo sapiens 224-233 8387950-9 1993 Preincubation of the cells with cycloheximide or actinomycin D totally abolished the up-regulatory effect of tumor necrosis factor on low-density lipoprotein receptors. Cycloheximide 32-45 tumor necrosis factor Homo sapiens 109-130 7680648-5 1993 Preincubation of the cells with cycloheximide "superinduced" the level of IL-8 mRNA stimulated by TNF alpha and IL-1 beta and RANTES mRNA stimulated by IL-1 beta, but decreased the expression of RANTES mRNA in response to TNF alpha. Cycloheximide 32-45 tumor necrosis factor Homo sapiens 98-107 7680648-5 1993 Preincubation of the cells with cycloheximide "superinduced" the level of IL-8 mRNA stimulated by TNF alpha and IL-1 beta and RANTES mRNA stimulated by IL-1 beta, but decreased the expression of RANTES mRNA in response to TNF alpha. Cycloheximide 32-45 tumor necrosis factor Homo sapiens 222-231 8439287-6 1993 However, inhibiting proliferation with cycloheximide resulted in increased sensitivity to TNF, implying that mitogenesis itself was not essential for a cytotoxic response. Cycloheximide 39-52 tumor necrosis factor Homo sapiens 90-93 7680009-5 1993 Cycloheximide, which abolished both the IFN gamma- and TNF alpha-induced increases in nitrite production, had no effect on the IFN gamma-induced increase in iNOS mRNA but markedly inhibited the TNF alpha-induced one. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 55-64 7680009-5 1993 Cycloheximide, which abolished both the IFN gamma- and TNF alpha-induced increases in nitrite production, had no effect on the IFN gamma-induced increase in iNOS mRNA but markedly inhibited the TNF alpha-induced one. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 194-203 8503951-4 1993 Interleukin-1 (IL-1) and, to a lesser extent, tumor necrosis factor alpha (TNF alpha) stimulated GM-CSF formation within 3 h; mRNA levels also increased particularly in the presence of the protein synthesis inhibitor, cycloheximide. Cycloheximide 218-231 tumor necrosis factor Homo sapiens 46-73 8503951-4 1993 Interleukin-1 (IL-1) and, to a lesser extent, tumor necrosis factor alpha (TNF alpha) stimulated GM-CSF formation within 3 h; mRNA levels also increased particularly in the presence of the protein synthesis inhibitor, cycloheximide. Cycloheximide 218-231 tumor necrosis factor Homo sapiens 75-84 8503951-5 1993 IL-1, TNF alpha and, in addition, interferon-gamma (IFN-gamma) raised the M-CSF levels within 6 h; cycloheximide potentiated the effects of IL-1 and TNF alpha on mRNA levels. Cycloheximide 99-112 tumor necrosis factor Homo sapiens 6-15 8503951-5 1993 IL-1, TNF alpha and, in addition, interferon-gamma (IFN-gamma) raised the M-CSF levels within 6 h; cycloheximide potentiated the effects of IL-1 and TNF alpha on mRNA levels. Cycloheximide 99-112 tumor necrosis factor Homo sapiens 149-158 8436829-7 1993 Of significance was the observation that cycloheximide could selectively modulate TNF-alpha mRNA transcription in neutrophils, depending on the cytokine used. Cycloheximide 41-54 tumor necrosis factor Homo sapiens 82-91 8447456-8 1993 Cycloheximide (an inhibitor of protein synthesis) attenuated the inhibitory effect of TNF-alpha and LPS on contractions to 5-hydroxytryptamine. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 86-95 8424834-7 1993 Use of cycloheximide and actinomycin D confirmed that TNF alpha was inducing MCP-1 expression at both the transcriptional and translational levels. Cycloheximide 7-20 tumor necrosis factor Homo sapiens 54-63 8430098-5 1993 Induction of EGFR mRNA expression by TNF-alpha was abrogated by cycloheximide but occurred independently of TNF-alpha-induced production of TGF-alpha protein. Cycloheximide 64-77 tumor necrosis factor Homo sapiens 37-46 1618817-8 1992 TNF-alpha-induced enhancement of LDL receptor gene expression was not observed when cycloheximide was present. Cycloheximide 84-97 tumor necrosis factor Homo sapiens 0-9 1292634-8 1992 In addition, experiments with the protein synthesis inhibitor cycloheximide suggested that the induction of mRNAs for both the heavy and light (beta 2-microglobulin) chains of the HLA class I antigen by TNF did not require de novo protein synthesis. Cycloheximide 62-75 tumor necrosis factor Homo sapiens 203-206 1445297-3 1992 In this paper we report that acute cytotoxicity elicited by TNF, in the presence of cycloheximide (CHX), also utilizes this pathway since inhibitors of lipoxygenase action fully prevent TNF/CHX killing of several cell lines. Cycloheximide 84-97 tumor necrosis factor Homo sapiens 60-63 1445297-3 1992 In this paper we report that acute cytotoxicity elicited by TNF, in the presence of cycloheximide (CHX), also utilizes this pathway since inhibitors of lipoxygenase action fully prevent TNF/CHX killing of several cell lines. Cycloheximide 84-97 tumor necrosis factor Homo sapiens 186-189 1445297-3 1992 In this paper we report that acute cytotoxicity elicited by TNF, in the presence of cycloheximide (CHX), also utilizes this pathway since inhibitors of lipoxygenase action fully prevent TNF/CHX killing of several cell lines. Cycloheximide 99-102 tumor necrosis factor Homo sapiens 60-63 1417842-1 1992 In this report we show that the adenovirus E3 region 14.7 kDa protein, heat and sodium arsenite, which have been defined previously as inhibitors of cytolysis, inhibit the tumor necrosis factor-alpha (TNF)-induced release of 3H-arachidonic acid from cycloheximide-sensitized C3HA fibroblasts. Cycloheximide 250-263 tumor necrosis factor Homo sapiens 172-199 1417842-1 1992 In this report we show that the adenovirus E3 region 14.7 kDa protein, heat and sodium arsenite, which have been defined previously as inhibitors of cytolysis, inhibit the tumor necrosis factor-alpha (TNF)-induced release of 3H-arachidonic acid from cycloheximide-sensitized C3HA fibroblasts. Cycloheximide 250-263 tumor necrosis factor Homo sapiens 201-204 1405321-10 1992 Inhibition studies with cycloheximide indicated de novo synthesis of TNF alpha. Cycloheximide 24-37 tumor necrosis factor Homo sapiens 69-78 1618860-10 1992 The rapid coordinate transcriptional regulation of C/EBP-alpha, GLUT4, and 422/aP2 by TNF in the presence of cycloheximide suggests that the TNF-induced loss of GLUT4 protein may be mediated by a post-translational modification of an existing transcription factor. Cycloheximide 109-122 tumor necrosis factor Homo sapiens 141-144 7678355-8 1993 The TNF-alpha-stimulated VCAM-1 expression is also inhibited by the PKC-specific inhibitor calphostin C. Protein synthesis inhibition with cycloheximide (CHX) and blocking of transcription with actinomycin D (ACT D) also inhibits the TNF-alpha and PMA-stimulated upregulation of VCAM-1. Cycloheximide 139-152 tumor necrosis factor Homo sapiens 4-13 7678355-8 1993 The TNF-alpha-stimulated VCAM-1 expression is also inhibited by the PKC-specific inhibitor calphostin C. Protein synthesis inhibition with cycloheximide (CHX) and blocking of transcription with actinomycin D (ACT D) also inhibits the TNF-alpha and PMA-stimulated upregulation of VCAM-1. Cycloheximide 154-157 tumor necrosis factor Homo sapiens 4-13 1333300-7 1992 The TNF-alpha-induced increase in VT-1 binding could be inhibited by simultaneous addition of the protein synthesis inhibitor cycloheximide. Cycloheximide 126-139 tumor necrosis factor Homo sapiens 4-13 1460427-11 1992 The addition of actinomycin D or cycloheximide to the HIV-infected monocytes before coculture reduced, > 2.5-fold, the levels of TNF-alpha. Cycloheximide 33-46 tumor necrosis factor Homo sapiens 132-141 1445297-3 1992 In this paper we report that acute cytotoxicity elicited by TNF, in the presence of cycloheximide (CHX), also utilizes this pathway since inhibitors of lipoxygenase action fully prevent TNF/CHX killing of several cell lines. Cycloheximide 99-102 tumor necrosis factor Homo sapiens 186-189 1445297-5 1992 Radical scavengers such as NAC and PDTC prevent TNF/CHX-induced cell killing and reduce MnSOD induction by TNF. Cycloheximide 52-55 tumor necrosis factor Homo sapiens 48-51 1739130-9 1992 Because heat-inactivated TNF-alpha failed to induce synthesis of IL-8 mRNA, and cycloheximide augmented TNF-alpha-induced synthesis, IL-8 expression appears to be a stimulus-specific primary induction phenomenon. Cycloheximide 80-93 tumor necrosis factor Homo sapiens 104-113 1339344-5 1992 In addition, binding of NF-jun to its recognition site is enhanced by treatment of cells with 12-O-tetradecanoylphorbol-13-acetate, tumor necrosis factor alpha or the protein synthesis inhibitor cycloheximide (CHX). Cycloheximide 210-213 tumor necrosis factor Homo sapiens 132-159 1577874-7 1992 The percentage of cells undergoing apoptosis depended on the concentration of TNF and was augmented by the addition of cycloheximide. Cycloheximide 119-132 tumor necrosis factor Homo sapiens 78-81 1577874-8 1992 A TNF-resistant variant derived from U937 did not undergo apoptosis in response to TNF, even in the presence of cycloheximide. Cycloheximide 112-125 tumor necrosis factor Homo sapiens 2-5 1345790-8 1992 Indeed, this direct cytotoxicity was completely abrogated by anti-TNF-alpha antibody and was sensitive to the metabolic inhibitors (cyclosporin A, CT, cycloheximide, and actinomycin D), all of which blocked CD4+/CD8+ T cell TNF-alpha production. Cycloheximide 151-164 tumor necrosis factor Homo sapiens 66-75 1732280-6 1992 Kinetic analysis demonstrated optimum TNF-alpha mRNA expression after a 4 h exposure to IL-1 beta, and peak TNF-alpha protein production at 18 h. Cycloheximide (CHX), an inhibitor of protein synthesis, markedly increased expression of TNF-alpha mRNA in IL-1 beta stimulated CH235-MG cells, indicating that de novo protein synthesis is not required for astroglioma TNF-alpha gene expression. Cycloheximide 146-159 tumor necrosis factor Homo sapiens 38-47 1732280-6 1992 Kinetic analysis demonstrated optimum TNF-alpha mRNA expression after a 4 h exposure to IL-1 beta, and peak TNF-alpha protein production at 18 h. Cycloheximide (CHX), an inhibitor of protein synthesis, markedly increased expression of TNF-alpha mRNA in IL-1 beta stimulated CH235-MG cells, indicating that de novo protein synthesis is not required for astroglioma TNF-alpha gene expression. Cycloheximide 146-159 tumor necrosis factor Homo sapiens 108-117 1732280-6 1992 Kinetic analysis demonstrated optimum TNF-alpha mRNA expression after a 4 h exposure to IL-1 beta, and peak TNF-alpha protein production at 18 h. Cycloheximide (CHX), an inhibitor of protein synthesis, markedly increased expression of TNF-alpha mRNA in IL-1 beta stimulated CH235-MG cells, indicating that de novo protein synthesis is not required for astroglioma TNF-alpha gene expression. Cycloheximide 146-159 tumor necrosis factor Homo sapiens 108-117 1732280-6 1992 Kinetic analysis demonstrated optimum TNF-alpha mRNA expression after a 4 h exposure to IL-1 beta, and peak TNF-alpha protein production at 18 h. Cycloheximide (CHX), an inhibitor of protein synthesis, markedly increased expression of TNF-alpha mRNA in IL-1 beta stimulated CH235-MG cells, indicating that de novo protein synthesis is not required for astroglioma TNF-alpha gene expression. Cycloheximide 146-159 tumor necrosis factor Homo sapiens 108-117 1732280-6 1992 Kinetic analysis demonstrated optimum TNF-alpha mRNA expression after a 4 h exposure to IL-1 beta, and peak TNF-alpha protein production at 18 h. Cycloheximide (CHX), an inhibitor of protein synthesis, markedly increased expression of TNF-alpha mRNA in IL-1 beta stimulated CH235-MG cells, indicating that de novo protein synthesis is not required for astroglioma TNF-alpha gene expression. Cycloheximide 161-164 tumor necrosis factor Homo sapiens 108-117 1732280-6 1992 Kinetic analysis demonstrated optimum TNF-alpha mRNA expression after a 4 h exposure to IL-1 beta, and peak TNF-alpha protein production at 18 h. Cycloheximide (CHX), an inhibitor of protein synthesis, markedly increased expression of TNF-alpha mRNA in IL-1 beta stimulated CH235-MG cells, indicating that de novo protein synthesis is not required for astroglioma TNF-alpha gene expression. Cycloheximide 161-164 tumor necrosis factor Homo sapiens 108-117 1732280-6 1992 Kinetic analysis demonstrated optimum TNF-alpha mRNA expression after a 4 h exposure to IL-1 beta, and peak TNF-alpha protein production at 18 h. Cycloheximide (CHX), an inhibitor of protein synthesis, markedly increased expression of TNF-alpha mRNA in IL-1 beta stimulated CH235-MG cells, indicating that de novo protein synthesis is not required for astroglioma TNF-alpha gene expression. Cycloheximide 161-164 tumor necrosis factor Homo sapiens 108-117 1345790-8 1992 Indeed, this direct cytotoxicity was completely abrogated by anti-TNF-alpha antibody and was sensitive to the metabolic inhibitors (cyclosporin A, CT, cycloheximide, and actinomycin D), all of which blocked CD4+/CD8+ T cell TNF-alpha production. Cycloheximide 151-164 tumor necrosis factor Homo sapiens 224-233 1370516-9 1992 The protein synthesis inhibitor cycloheximide (Cy) blocked IL-1-, TNF-, or LPS-induced MCP gene expression in monocytes. Cycloheximide 32-45 tumor necrosis factor Homo sapiens 66-69 1370516-9 1992 The protein synthesis inhibitor cycloheximide (Cy) blocked IL-1-, TNF-, or LPS-induced MCP gene expression in monocytes. Cycloheximide 47-49 tumor necrosis factor Homo sapiens 66-69 1370465-2 1992 Differential screening of a TNF-stimulated, cycloheximide-treated human umbilical vein endothelial cell library has resulted in the cloning of several novel cDNAs whose protein products are involved in the primary response of the endothelium to TNF. Cycloheximide 44-57 tumor necrosis factor Homo sapiens 28-31 1370465-2 1992 Differential screening of a TNF-stimulated, cycloheximide-treated human umbilical vein endothelial cell library has resulted in the cloning of several novel cDNAs whose protein products are involved in the primary response of the endothelium to TNF. Cycloheximide 44-57 tumor necrosis factor Homo sapiens 245-248 1730604-3 1992 We find, however, that in the presence of either actinomycin D (Act D) or cycloheximide (CHI), TNF is indeed able to induce phospholipase activity and that the TNF-induced activation of PLA2 occurs 2-4 h before the onset of 51Cr release. Cycloheximide 74-87 tumor necrosis factor Homo sapiens 95-98 1730604-3 1992 We find, however, that in the presence of either actinomycin D (Act D) or cycloheximide (CHI), TNF is indeed able to induce phospholipase activity and that the TNF-induced activation of PLA2 occurs 2-4 h before the onset of 51Cr release. Cycloheximide 74-87 tumor necrosis factor Homo sapiens 160-163 1571090-4 1992 The suppressive effects of IL-4 appear to be dependent upon de novo protein synthesis, as cycloheximide abrogated the IL-4-induced reduction in TNF-alpha mRNA levels from PBM. Cycloheximide 90-103 tumor necrosis factor Homo sapiens 144-153 1939146-1 1991 Pretreatment of HT-1080 fibrosarcoma cells with tumor necrosis factor (TNF) induced resistance to the cytolytic activity of this cytokine in combination with cycloheximide. Cycloheximide 158-171 tumor necrosis factor Homo sapiens 48-69 1744113-5 1991 When protein synthesis was inhibited by cycloheximide during TPA pretreatment, TNF no more enhanced the Mn-SOD mRNA accumulation. Cycloheximide 40-53 tumor necrosis factor Homo sapiens 79-82 1939146-1 1991 Pretreatment of HT-1080 fibrosarcoma cells with tumor necrosis factor (TNF) induced resistance to the cytolytic activity of this cytokine in combination with cycloheximide. Cycloheximide 158-171 tumor necrosis factor Homo sapiens 71-74 1874802-6 1991 Based upon studies with cycloheximide, de novo protein biosynthesis was required for TNF-mediated ODC induction in ME-180 cells. Cycloheximide 24-37 tumor necrosis factor Homo sapiens 85-88 1918980-8 1991 To determine if protein synthesis was required for induction of Il-1 beta gene expression, we treated PMN simultaneously with cytokines and cycloheximide, and found that cycloheximide enhanced the accumulation of Il-1-induced Il-1 beta mRNA, but abrogated the accumulation of Il-1 beta mRNA, by TNF- or TNF plus Il-1-treated PMN. Cycloheximide 170-183 tumor necrosis factor Homo sapiens 295-298 1918980-8 1991 To determine if protein synthesis was required for induction of Il-1 beta gene expression, we treated PMN simultaneously with cytokines and cycloheximide, and found that cycloheximide enhanced the accumulation of Il-1-induced Il-1 beta mRNA, but abrogated the accumulation of Il-1 beta mRNA, by TNF- or TNF plus Il-1-treated PMN. Cycloheximide 170-183 tumor necrosis factor Homo sapiens 303-306 1909330-7 1991 The TA1-R6 cells, however, are capable of incorporating exogenous 20:4 into PC and PE, and when loaded in such manner they become significantly more sensitive to the cytotoxic effects of TNF in the presence of cycloheximide. Cycloheximide 210-223 tumor necrosis factor Homo sapiens 187-190 1856599-6 1991 Antigenic and bioactive IL-8 were significantly apparent by 4-8 h, respectively, and increased significantly to maximal levels by 24 h. Furthermore, adherent PBMC IL-8 gene expression was suppressed by either concomitant treatment with actinomycin-D or cycloheximide, yet specific neutralizing antibodies directed against either IL-1 beta or tumor necrosis factor (TNF)-alpha failed to alter adherence-induced steady-state IL-8 mRNA levels. Cycloheximide 253-266 tumor necrosis factor Homo sapiens 342-375 1653047-5 1991 Inhibition of protein synthesis by cycloheximide prevented the primary effect of TNF. Cycloheximide 35-48 tumor necrosis factor Homo sapiens 81-84 2121799-8 1990 Furthermore, astrocyte class II mRNA expression was inhibited when cycloheximide (CHX) was added together with IFN-gamma or IFN-gamma/TNF-alpha, and when CHX was added up to 4 h after treatment with IFN-gamma or IFN-gamma/TNF-alpha. Cycloheximide 67-80 tumor necrosis factor Homo sapiens 222-231 1672341-5 1991 In addition, although coincubation of HER2/neu-expressing targets with cycloheximide resulted in significant TNF-induced lysis, when compared to HER2/neu-nonexpressing targets similarly treated with cycloheximide, a significant relative resistance was still present. Cycloheximide 71-84 tumor necrosis factor Homo sapiens 109-112 1846880-3 1991 The more pronounced effects of TNF were accompanied by an augmented surface membrane depolarization rate and were insensitive to both pertussis toxin and calcium ion chelation, but were negated by concomitant incubation with puromycin or cycloheximide during priming. Cycloheximide 238-251 tumor necrosis factor Homo sapiens 31-34 1801706-7 1991 The induction of uPA by TNF was inhibited by actinomycin D and cycloheximide implying the necessity of RNA and protein synthesis, respectively. Cycloheximide 63-76 tumor necrosis factor Homo sapiens 24-27 1905388-5 1991 Maximal TNF release occurred at 8 h of LPS stimulation, and required both protein and RNA synthesis as evidenced by the ability of both actinomycin D and cycloheximide to inhibit its release. Cycloheximide 154-167 tumor necrosis factor Homo sapiens 8-11 1986224-4 1991 NF-kappa B activation by TNF alpha was initially cycloheximide insensitive, but maintenance of NF-kappa B activity required ongoing protein synthesis and continuous stimulation by TNF alpha. Cycloheximide 49-62 tumor necrosis factor Homo sapiens 25-34 2121799-8 1990 Furthermore, astrocyte class II mRNA expression was inhibited when cycloheximide (CHX) was added together with IFN-gamma or IFN-gamma/TNF-alpha, and when CHX was added up to 4 h after treatment with IFN-gamma or IFN-gamma/TNF-alpha. Cycloheximide 82-85 tumor necrosis factor Homo sapiens 222-231 1700731-7 1990 The transcription inhibitor, actinomycin D, and protein synthesis inhibitor, cycloheximide, inhibited the increase in GM-CSF and G-CSF production induced by IL-1 and TNF. Cycloheximide 77-90 tumor necrosis factor Homo sapiens 166-169 2226778-7 1990 Stimulation of IL-6 transcripts in fibroblasts did also not require new protein synthesis as exposure to the protein synthesis inhibitor cycloheximide (CHX) enhanced accumulation of IL-6 mRNA in the presence or absence of TNF-alpha or LT. Cycloheximide 137-150 tumor necrosis factor Homo sapiens 222-231 2233719-1 1990 We have previously described the cloning of a group of novel cellular immediate-early response genes whose expression in human umbilical vein endothelial cells is induced by tumor necrosis factor alpha in the presence of cycloheximide. Cycloheximide 221-234 tumor necrosis factor Homo sapiens 174-201 2104238-4 1990 It was found that early pretreatment with cycloheximide interferes with TNF-alpha mRNA induction by Staphylococcus aureus. Cycloheximide 42-55 tumor necrosis factor Homo sapiens 72-81 2226778-7 1990 Stimulation of IL-6 transcripts in fibroblasts did also not require new protein synthesis as exposure to the protein synthesis inhibitor cycloheximide (CHX) enhanced accumulation of IL-6 mRNA in the presence or absence of TNF-alpha or LT. Cycloheximide 152-155 tumor necrosis factor Homo sapiens 222-231 2406243-9 1990 On exposure of endothelial cells to TNF there is a rapid and substantial increase in levels of mRNA encoding the six genes, which are further superinduced by cycloheximide. Cycloheximide 158-171 tumor necrosis factor Homo sapiens 36-39 2382730-0 1990 Enhancement of tumor necrosis factor-induced endothelial cell injury by cycloheximide. Cycloheximide 72-85 tumor necrosis factor Homo sapiens 15-36 2382730-3 1990 We now report that cycloheximide (CHX), an inhibitor of protein synthesis, renders endothelial cells highly susceptible to TNF-induced lysis. Cycloheximide 19-32 tumor necrosis factor Homo sapiens 123-126 2382730-3 1990 We now report that cycloheximide (CHX), an inhibitor of protein synthesis, renders endothelial cells highly susceptible to TNF-induced lysis. Cycloheximide 34-37 tumor necrosis factor Homo sapiens 123-126 2354999-7 1990 There was also no evidence of superinduction of mRNA in peripheral blood mononuclear cells stimulated with LPS, whereas, tumor necrosis factor alpha mRNA was elevated in the presence of cycloheximide. Cycloheximide 186-199 tumor necrosis factor Homo sapiens 121-148 2155279-7 1990 These findings suggested that MT disassembly was responsible for the observed downregulation of TNF-alpha R. The protein synthesis inhibitor cycloheximide inhibited binding of TNF-alpha to a similar extent and with a similar time course as colchicine in the absence of added ligand. Cycloheximide 141-154 tumor necrosis factor Homo sapiens 96-105 2155279-7 1990 These findings suggested that MT disassembly was responsible for the observed downregulation of TNF-alpha R. The protein synthesis inhibitor cycloheximide inhibited binding of TNF-alpha to a similar extent and with a similar time course as colchicine in the absence of added ligand. Cycloheximide 141-154 tumor necrosis factor Homo sapiens 176-185 2334910-4 1990 With either TNF or IL-1 beta as the stimulus, TNF mRNA is induced first, peaks within 1-3 h, and declines to nearly undetectable levels by 9 h. TNF mRNA accumulation is enhanced in the presence of cycloheximide indicating that de novo protein synthesis is not required for maximal TNF mRNA induction. Cycloheximide 197-210 tumor necrosis factor Homo sapiens 12-15 2334910-4 1990 With either TNF or IL-1 beta as the stimulus, TNF mRNA is induced first, peaks within 1-3 h, and declines to nearly undetectable levels by 9 h. TNF mRNA accumulation is enhanced in the presence of cycloheximide indicating that de novo protein synthesis is not required for maximal TNF mRNA induction. Cycloheximide 197-210 tumor necrosis factor Homo sapiens 46-49 2334910-4 1990 With either TNF or IL-1 beta as the stimulus, TNF mRNA is induced first, peaks within 1-3 h, and declines to nearly undetectable levels by 9 h. TNF mRNA accumulation is enhanced in the presence of cycloheximide indicating that de novo protein synthesis is not required for maximal TNF mRNA induction. Cycloheximide 197-210 tumor necrosis factor Homo sapiens 46-49 2334910-4 1990 With either TNF or IL-1 beta as the stimulus, TNF mRNA is induced first, peaks within 1-3 h, and declines to nearly undetectable levels by 9 h. TNF mRNA accumulation is enhanced in the presence of cycloheximide indicating that de novo protein synthesis is not required for maximal TNF mRNA induction. Cycloheximide 197-210 tumor necrosis factor Homo sapiens 46-49 2509363-3 1989 TNF-induced resistance to chlamydiae could be blocked with cycloheximide, suggesting that it involves the function of some induced proteins. Cycloheximide 59-72 tumor necrosis factor Homo sapiens 0-3 2105339-4 1990 The combination of a protein synthesis inhibitor, cycloheximide, and TNF increased levels of CSF-1 mRNA compared with treatment by TNF alone. Cycloheximide 50-63 tumor necrosis factor Homo sapiens 131-134 2322985-0 1990 Cycloheximide-induced modulation of TNF-mediated cytotoxicity in sensitive and resistant ovarian tumor cells. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 36-39 2322985-11 1990 Cells pretreated with CHX for 24 h showed poor binding of [125]I-TNF and poor internalization, whereas cells pretreated for 24 h with TNF showed marked enhancement of internalization. Cycloheximide 22-25 tumor necrosis factor Homo sapiens 65-68 2322985-12 1990 The sensitivity of freshly derived ovarian carcinoma lines to TNF and CHX demonstrated that TNF-resistant cells became more sensitive if treated with CHX. Cycloheximide 70-73 tumor necrosis factor Homo sapiens 92-95 2555368-7 1989 Treatment of cells with cycloheximide stabilized tissue factor and PAI-2 mRNAs and increased their induction by PMA or TNF. Cycloheximide 24-37 tumor necrosis factor Homo sapiens 119-122 2925656-2 1989 TNF is not toxic to either adipocytes or preadipocytes when used alone but is highly toxic to these cells when used in conjunction with cycloheximide, yielding virtually 100% killing within 4-6 h of treatment. Cycloheximide 136-149 tumor necrosis factor Homo sapiens 0-3 2559490-6 1989 Cycloheximide inhibited the induction of PCA by THP-1 cells, which shows that the protein synthesis is essential to mediate the effect of TNF-alpha. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 138-147 2476237-1 1989 Tumor necrosis factor (TNF) induces the synthesis of protein(s) that can protect cells against subsequent killing by TNF in the presence of cycloheximide. Cycloheximide 140-153 tumor necrosis factor Homo sapiens 0-21 2476237-1 1989 Tumor necrosis factor (TNF) induces the synthesis of protein(s) that can protect cells against subsequent killing by TNF in the presence of cycloheximide. Cycloheximide 140-153 tumor necrosis factor Homo sapiens 23-26 2476237-1 1989 Tumor necrosis factor (TNF) induces the synthesis of protein(s) that can protect cells against subsequent killing by TNF in the presence of cycloheximide. Cycloheximide 140-153 tumor necrosis factor Homo sapiens 117-120 2506186-4 1989 We investigated the molecular basis for these diverse actions of TNF by differential screening of a cDNA library prepared from TNF and cycloheximide-treated human umbilical vein endothelial (HUVE) cells. Cycloheximide 135-148 tumor necrosis factor Homo sapiens 65-68 2785770-5 1989 Moreover, perfusion with 20-100 micrograms/ml cycloheximide, an inhibitor of protein synthesis, blocked the TNF-induced impairment of the relaxation to ACh. Cycloheximide 46-59 tumor necrosis factor Homo sapiens 108-111 2925656-6 1989 The adipocyte differentiation-inducing agents, dexamethasone and indomethacin, block the cytotoxicity induced by TNF alone in the TA1 R-6 line but do not block the rapid cytotoxicity of TNF and cycloheximide in the parental line. Cycloheximide 194-207 tumor necrosis factor Homo sapiens 113-116 2785495-8 1989 Cycloheximide (Cy) inhibited the production of TNF-alpha. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 47-56 2785495-8 1989 Cycloheximide (Cy) inhibited the production of TNF-alpha. Cycloheximide 0-2 tumor necrosis factor Homo sapiens 47-56 2839482-2 1988 With receptor synthesis inhibited by cycloheximide, the half-life of the surface TNF receptor was 2 h in the absence of TNF and 30 min in its presence, suggesting that the TNF receptor is non-recycling and that its internalization is accelerated by TNF. Cycloheximide 37-50 tumor necrosis factor Homo sapiens 81-84 3194703-10 1988 The release was inhibited by cycloheximide but not by actinomycin D, indicating that the TNF detected did not represent TNF present in vivo. Cycloheximide 29-42 tumor necrosis factor Homo sapiens 89-92 3261295-6 1988 This activity of TNF is inhibited by treating endothelial cells with the inhibitors of protein or RNA synthesis cycloheximide or actinomycin D. Cycloheximide 112-125 tumor necrosis factor Homo sapiens 17-20 2839482-3 1988 During cell incubation with TNF receptor degradation suppressed by chloroquine, the number of surface TNF receptors remained approximately constant, but the total number of surface and internal TNF receptors increased gradually, at 3 h reaching 1.5 times the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Cycloheximide 401-414 tumor necrosis factor Homo sapiens 28-31 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 56-69 tumor necrosis factor Homo sapiens 88-91 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 56-69 tumor necrosis factor Homo sapiens 123-126 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 56-69 tumor necrosis factor Homo sapiens 123-126 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 56-69 tumor necrosis factor Homo sapiens 123-126 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 56-69 tumor necrosis factor Homo sapiens 123-126 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 268-281 tumor necrosis factor Homo sapiens 123-126 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 268-281 tumor necrosis factor Homo sapiens 123-126 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 268-281 tumor necrosis factor Homo sapiens 123-126 2839482-5 1988 During incubations with protein synthesis suppressed by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in number to a peak at 60 min and gradually decreasing, and cells previously exposed to cycloheximide with or without TNF showed no recurrence of surface TNF receptors, suggesting that the TNF receptor is non-recycling. Cycloheximide 268-281 tumor necrosis factor Homo sapiens 123-126 3258601-11 1988 Cycloheximide (0.1 mM), an inhibitor of protein synthesis, blocked the inhibitory effect of both TNF alpha and interleukin-1 on procollagen alpha 1(I) mRNA. Cycloheximide 0-13 tumor necrosis factor Homo sapiens 97-106 2828427-7 1988 Furthermore, both sensitive and resistant epithelial tumor cells had the capacity to express TNF transcripts in the presence of the protein synthesis inhibitor, cycloheximide. Cycloheximide 161-174 tumor necrosis factor Homo sapiens 93-96 2834347-5 1987 Following removal of TNF from growth medium, binding activity was restored within 3 h. Cycloheximide prevented the restoration of TNF receptors, suggesting that de novo synthesis of receptors was required to restore the binding activity. Cycloheximide 87-100 tumor necrosis factor Homo sapiens 130-133 2829746-2 1988 With receptor synthesis inhibited by cycloheximide, the half-life of the surface TNF receptor was 2h in the absence of TNF and 30min in its presence, suggesting that the TNF receptor was non-recycling and that its internalization was accelerated by TNF. Cycloheximide 37-50 tumor necrosis factor Homo sapiens 81-84 2829746-3 1988 During cell incubation with suppression of TNF receptor degradation by chloroquine, the number of surface TNF receptors remained approximately constants, but the total number of surface and internal TNF receptors increased gradually, at 3h reaching 1.5 times of the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Cycloheximide 408-421 tumor necrosis factor Homo sapiens 43-46 2829746-6 1988 In incubation with suppression of protein synthesis by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in the number to a peak level at 60 min and gradually decreasing. Cycloheximide 55-68 tumor necrosis factor Homo sapiens 87-90 2829746-6 1988 In incubation with suppression of protein synthesis by cycloheximide following surface TNF receptor digestion by trypsin, TNF receptors reappeared on the cell surface, increasing in the number to a peak level at 60 min and gradually decreasing. Cycloheximide 55-68 tumor necrosis factor Homo sapiens 122-125 3276786-4 1988 We observed that the IFN-beta 2 gene is transcribed at a low level in uninduced FS-4 cells and that this transcriptional activity is increased 2- to 3-fold in cycloheximide-treated cells, 20- to 35-fold in IL-1 alpha-treated cells, and 5- to 15-fold in TNF-treated cells. Cycloheximide 159-172 tumor necrosis factor Homo sapiens 253-256 3246539-3 1988 Artificial inhibition of either RNA or protein synthesis by L-M cells, by addition of actinomycin D or cycloheximide, increased the cytotoxic effect of TNF and thus suggested that the elevated RNA and protein synthesis is related not to the cytotoxic reaction itself but rather to a defense mechanism. Cycloheximide 103-116 tumor necrosis factor Homo sapiens 152-155 3594575-1 1987 Tumor necrosis factor (TNF) is cytocidal for human and murine cells when protein synthesis is inhibited by cycloheximide, but some protease inhibitors completely protect these cells from TNF cytotoxicity. Cycloheximide 107-120 tumor necrosis factor Homo sapiens 0-21 3594575-1 1987 Tumor necrosis factor (TNF) is cytocidal for human and murine cells when protein synthesis is inhibited by cycloheximide, but some protease inhibitors completely protect these cells from TNF cytotoxicity. Cycloheximide 107-120 tumor necrosis factor Homo sapiens 23-26