PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 interleukin 1 alpha Homo sapiens 40-59 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 interleukin 1 alpha Homo sapiens 61-70 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 interleukin 1 alpha Homo sapiens 40-59 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 interleukin 1 alpha Homo sapiens 61-70 18387309-2 2008 The aim of the presented work was to analyze the mechanism of IL-1-induced cytocidal effect in HeLa cells in the presence of cycloheximide (CHX). Cycloheximide 125-138 interleukin 1 alpha Homo sapiens 62-66 18729741-4 2008 Cycloheximide treatment indicated that the augmenting effect of CSC on IL-1alpha, IL-1beta and IL-8, but not IL-6 and CYP1A1, mRNA expression requires de novo protein synthesis. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 71-80 18387309-2 2008 The aim of the presented work was to analyze the mechanism of IL-1-induced cytocidal effect in HeLa cells in the presence of cycloheximide (CHX). Cycloheximide 140-143 interleukin 1 alpha Homo sapiens 62-66 10896254-7 2000 Cycloheximide treatment of HUVEC slightly inhibited the IL-1alpha-induced expression of VEGF mRNA, and IL-1alpha may mediate, at least in part, VEGF expression in response to IL-1alpha. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 56-65 16121032-10 2005 In keeping with this observation, the protein synthesis inhibitor cycloheximide abolished the stimulatory effect of IL-1 on ATPase-mediated extrusion. Cycloheximide 66-79 interleukin 1 alpha Homo sapiens 116-120 9661070-8 1998 Cycloheximide enhanced effects of both IL-1 and PMA, suggesting that de novo protein synthesis is not required for induction of PGHS-2. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 39-51 10385262-6 1999 IL-1alpha-dependent receptor induction was blocked by cycloheximide. Cycloheximide 54-67 interleukin 1 alpha Homo sapiens 0-9 8796788-5 1996 The action of IL-1 was greatly potentiated by the protein kinase C-activating phorbol ester, TPA, and inhibited by actinomycin D and cycloheximide. Cycloheximide 133-146 interleukin 1 alpha Homo sapiens 14-18 8886420-14 1996 Experiments using cycloheximide demonstrated that this synergistic effect of IL-13 and IL-1 alpha on IL-8 secretion was not through de novo protein synthesis. Cycloheximide 18-31 interleukin 1 alpha Homo sapiens 87-97 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 interleukin 1 alpha Homo sapiens 71-81 7675826-3 1995 Application of 10 ng/ml IL-1 alpha increased the production of PGF2 alpha for 2-24 h. Coincubation of IL-1 alpha with actinomycin D (1 microgram/ml) or cycloheximide (10 micrograms/ml) completely blocked the increase in PGF2 alpha. Cycloheximide 152-165 interleukin 1 alpha Homo sapiens 24-34 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 interleukin 1 alpha Homo sapiens 19-29 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 interleukin 1 alpha Homo sapiens 19-29 8680718-9 1995 6 Studies with IL-1 alpha/IFN-gamma combination demonstrated a time dependent expression of iNOS mRNA, first observed at 6 h, peaked at 24 h and was undetectable by 72 h. IL-1 alpha (0.3-10 ng ml-1) and IFN-gamma (10-300 u ml-1) in combination induced a concentration-dependent expression of iNOS mRNA at 24 h. 7 Pretreatment with cycloheximide before IL-1 alpha/IFN-gamma stimulation reduced nitrite levels to basal values. Cycloheximide 331-344 interleukin 1 alpha Homo sapiens 15-25 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 interleukin 1 alpha Homo sapiens 249-259 7861725-7 1994 Cycloheximide and actinomycin D blocked the production of IL-1 alpha and -beta protein, showing that de novo production of IL-1 or synthesis of mRNA stabilizing proteins are needed after stimulation. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 58-78 7861725-7 1994 Cycloheximide and actinomycin D blocked the production of IL-1 alpha and -beta protein, showing that de novo production of IL-1 or synthesis of mRNA stabilizing proteins are needed after stimulation. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 58-62 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 interleukin 1 alpha Homo sapiens 249-259 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 interleukin 1 alpha Homo sapiens 249-259 8147926-6 1994 RESULTS: IL-1 induced an increase in COX activity (as assessed by prostaglandin E2 release) that was dose- and time-dependent and was blocked by cycloheximide, actinomycin D, and dexamethasone. Cycloheximide 145-158 interleukin 1 alpha Homo sapiens 9-13 8131794-1 1993 In an attempt to understand more directly the molecular mechanisms involved in the cellular response of endothelial cells to Interleukin-1 (IL-1), we have made several cDNA libraries from human umbilical vein endothelial cells (HUVEC) stimulated for 1 h with IL-1 in the presence of cycloheximide. Cycloheximide 283-296 interleukin 1 alpha Homo sapiens 140-144 8288917-8 1994 Dexamethasone (10 nM), and the protein synthesis inhibitors actinomycin D (1 microM) and cycloheximide (3 micrograms/ml) completely abolished the effect of interleukin-1 on 15-HETE formation. Cycloheximide 89-102 interleukin 1 alpha Homo sapiens 156-169 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 interleukin 1 alpha Homo sapiens 15-19 8347686-6 1993 Actinomycin D and cycloheximide inhibited both the basal and IL-1 alpha-induced production of M-CSF, suggesting a requirement for de novo RNA and protein synthesis. Cycloheximide 18-31 interleukin 1 alpha Homo sapiens 61-71 8373725-7 1993 On the other hand, interleukin-1 amplification of bradykinin-stimulated release of arachidonic acid was blocked by actinomycin D and cycloheximide. Cycloheximide 133-146 interleukin 1 alpha Homo sapiens 19-32 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 interleukin 1 alpha Homo sapiens 0-4 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 interleukin 1 alpha Homo sapiens 140-144 1636747-8 1992 By utilizing stable isotope methods, we could demonstrate that IL-1 increased free arachidonate levels, implying new PLA2 synthesis over a time course that was maximal at 6 h and was cycloheximide and actinomycin D sensitive. Cycloheximide 183-196 interleukin 1 alpha Homo sapiens 63-67 8425199-6 1993 IL-1 caused a time- and dose-dependent increase in 125I-labeled IFN-gamma binding that was maximal at 6 h, persisted for at least 24 h, and was blocked by both actinomycin D and cycloheximide. Cycloheximide 178-191 interleukin 1 alpha Homo sapiens 0-4 8425199-8 1993 IL-1 also produced a time- and dose-dependent increase in IFN-gamma receptor mRNA levels that was maximal at 3 h and persisted for at least 24 h. Actinomycin D, but not cycloheximide, completely blocked the IL-1-mediated increase in IFN-gamma receptor mRNA levels. Cycloheximide 169-182 interleukin 1 alpha Homo sapiens 0-4 1426065-3 1992 The combination of cycloheximide and recombinant interleukin-1 caused a 14-fold enhancement of interleukin-1 alpha and interleukin-1 beta mRNA expression above that observed after cells were stimulated with interleukin-1 alone. Cycloheximide 19-32 interleukin 1 alpha Homo sapiens 95-108 1426065-3 1992 The combination of cycloheximide and recombinant interleukin-1 caused a 14-fold enhancement of interleukin-1 alpha and interleukin-1 beta mRNA expression above that observed after cells were stimulated with interleukin-1 alone. Cycloheximide 19-32 interleukin 1 alpha Homo sapiens 95-108 1584804-8 1992 IL-1 mRNA accumulates in young fibroblasts treated with cycloheximide, suggesting that it is transcribed but unstable in these cells; accumulation of IL-1 mRNA in old fibroblasts may be due at least in part to increased stability. Cycloheximide 56-69 interleukin 1 alpha Homo sapiens 0-4 1610348-5 1992 When IL-1 alpha-induced fibroblasts were exposed to cycloheximide there was enhancement of the net de novo synthesis and secretion of IL-6 as followed by [35S]-methionine labeling ("superinduction") but the secreted cytokine was no longer phosphorylated as monitored by [32P] labeling. Cycloheximide 52-65 interleukin 1 alpha Homo sapiens 5-15 1319454-8 1992 The effect of IL-1 took 2 h to develop and was blocked by cycloheximide (100 mumol/l). Cycloheximide 58-71 interleukin 1 alpha Homo sapiens 14-18 1892733-9 1991 Cycloheximide and actinomycin D inhibited the stimulation of arachidonic acid release by IL-1, PMA or DiC8. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 89-93 1370516-9 1992 The protein synthesis inhibitor cycloheximide (Cy) blocked IL-1-, TNF-, or LPS-induced MCP gene expression in monocytes. Cycloheximide 32-45 interleukin 1 alpha Homo sapiens 59-63 1370516-9 1992 The protein synthesis inhibitor cycloheximide (Cy) blocked IL-1-, TNF-, or LPS-induced MCP gene expression in monocytes. Cycloheximide 47-49 interleukin 1 alpha Homo sapiens 59-63 2053915-5 1991 Cycloheximide and actinomycin D caused a concentration-dependent suppression of the PDGF-BB-mediated potentiation of radiolabeled IL-1 alpha binding to RAC and cell responsiveness to IL-1 alpha. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 130-140 2053915-5 1991 Cycloheximide and actinomycin D caused a concentration-dependent suppression of the PDGF-BB-mediated potentiation of radiolabeled IL-1 alpha binding to RAC and cell responsiveness to IL-1 alpha. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 183-193 2033250-9 1991 The protein synthesis inhibitors puromycin, emetine, and cycloheximide also blocked the decline in pP29 during IL-1 treatment. Cycloheximide 57-70 interleukin 1 alpha Homo sapiens 111-115 1717608-9 1991 Cycloheximide partially reduces the increased conversion but completely blocks interleukin-1-induced release of prostaglandin E2 from intact cells. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 79-92 1892733-10 1991 The addition of cycloheximide or actinomycin D 15-45 min after IL-1 also inhibited IL-1 stimulated arachidonic acid release, indicating that continued protein synthesis was required for IL-1 action. Cycloheximide 16-29 interleukin 1 alpha Homo sapiens 63-67 1892733-10 1991 The addition of cycloheximide or actinomycin D 15-45 min after IL-1 also inhibited IL-1 stimulated arachidonic acid release, indicating that continued protein synthesis was required for IL-1 action. Cycloheximide 16-29 interleukin 1 alpha Homo sapiens 83-87 1892733-10 1991 The addition of cycloheximide or actinomycin D 15-45 min after IL-1 also inhibited IL-1 stimulated arachidonic acid release, indicating that continued protein synthesis was required for IL-1 action. Cycloheximide 16-29 interleukin 1 alpha Homo sapiens 83-87 1694171-3 1990 Our data demonstrate that 1) the Cox mRNA is expressed at low levels in untreated cells; 2) IL-1 alpha induces the Cox mRNA within 2 h, and this induction is sustained for more than 24 h; 3) IL-1 alpha induction is dose-dependent; 4) cycloheximide potentiates the induction of the Cox mRNA by IL-1 alpha while actinomycin D prevents the induction, and 5) IL-1 alpha also stimulates Cox production in a time-dependent fashion which correlates with the increase in prostacyclin synthesis. Cycloheximide 234-247 interleukin 1 alpha Homo sapiens 92-102 2124239-9 1990 In separate studies on the effect of IL-1 on AA mobilization, we found that IL-1 induced an increase in phospholipase A2 (PLA2) activity and that cycloheximide blocked the increase, suggesting the requirement for new protein synthesis. Cycloheximide 146-159 interleukin 1 alpha Homo sapiens 37-41 2254900-2 1990 Pretreatment of chondrocytes with actinomycin D or cycloheximide significantly inhibited IL-1 induced PLA2 activation and secretion, suggesting that the enzyme induction process is RNA and protein synthesis dependent. Cycloheximide 51-64 interleukin 1 alpha Homo sapiens 89-93 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 interleukin 1 alpha Homo sapiens 157-161 1694171-3 1990 Our data demonstrate that 1) the Cox mRNA is expressed at low levels in untreated cells; 2) IL-1 alpha induces the Cox mRNA within 2 h, and this induction is sustained for more than 24 h; 3) IL-1 alpha induction is dose-dependent; 4) cycloheximide potentiates the induction of the Cox mRNA by IL-1 alpha while actinomycin D prevents the induction, and 5) IL-1 alpha also stimulates Cox production in a time-dependent fashion which correlates with the increase in prostacyclin synthesis. Cycloheximide 234-247 interleukin 1 alpha Homo sapiens 191-201 1694171-3 1990 Our data demonstrate that 1) the Cox mRNA is expressed at low levels in untreated cells; 2) IL-1 alpha induces the Cox mRNA within 2 h, and this induction is sustained for more than 24 h; 3) IL-1 alpha induction is dose-dependent; 4) cycloheximide potentiates the induction of the Cox mRNA by IL-1 alpha while actinomycin D prevents the induction, and 5) IL-1 alpha also stimulates Cox production in a time-dependent fashion which correlates with the increase in prostacyclin synthesis. Cycloheximide 234-247 interleukin 1 alpha Homo sapiens 191-201 1694171-3 1990 Our data demonstrate that 1) the Cox mRNA is expressed at low levels in untreated cells; 2) IL-1 alpha induces the Cox mRNA within 2 h, and this induction is sustained for more than 24 h; 3) IL-1 alpha induction is dose-dependent; 4) cycloheximide potentiates the induction of the Cox mRNA by IL-1 alpha while actinomycin D prevents the induction, and 5) IL-1 alpha also stimulates Cox production in a time-dependent fashion which correlates with the increase in prostacyclin synthesis. Cycloheximide 234-247 interleukin 1 alpha Homo sapiens 191-201 2406172-7 1990 Using the amnion cells in primary monolayer culture to investigate the regulation of preproendothelin mRNA expression, we found that epidermal growth factor (EGF) and interleukin-1 (IL-1) act to stimulate preproendothelin mRNA levels; in addition, the induction of preproendothelin mRNA by either of these agents is enhanced upon simultaneous treatment with cycloheximide. Cycloheximide 358-371 interleukin 1 alpha Homo sapiens 133-186 1693636-8 1990 The anti-LFA-3-mediated augmentation of IL-1 release required both new protein and RNA synthesis as shown by the ability of cycloheximide and actinomycin-D to inhibit augmentation of IL-1 production by TE cells, and by direct quantitation of IL-1 alpha and IL-1 beta mRNA by Northern blot analysis. Cycloheximide 124-137 interleukin 1 alpha Homo sapiens 242-252 2787453-10 1989 In contrast, no IL-1 beta message was detectable, not even after treatment of the cells with phorbol ester or cycloheximide, which resulted in approximately 5-fold enhancement of IL-1 alpha mRNA expression. Cycloheximide 110-123 interleukin 1 alpha Homo sapiens 179-189 2295836-4 1990 Increased PGE2 synthesis in response to IL-1 was inhibited by cycloheximide, suggesting a requirement for new protein synthesis. Cycloheximide 62-75 interleukin 1 alpha Homo sapiens 40-44 2557044-8 1989 However, we found that cycloheximide, when added to synovial fibroblast cultures up to 6 hours after treatment with IL-1, inhibited the expression of collagenase mRNA. Cycloheximide 23-36 interleukin 1 alpha Homo sapiens 116-120 2785335-2 1989 IL 1 induced PMN leukocyte accumulation that was slow in onset, reaching a peak rate at 3-4 h and that was inhibitable by Actinomycin D and Cycloheximide. Cycloheximide 140-153 interleukin 1 alpha Homo sapiens 0-4 2552772-0 1989 Cycloheximide inhibits the induction of collagenase mRNA in chondrocytes exposed to synovial factors or recombinant interleukin-1. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 116-129 2527495-7 1989 The turnover of the Raji IL-1 receptor, measured by inhibiting protein synthesis with cycloheximide, was much faster than that of the EL4 IL-1 receptor, with a half-time of 2 h as against 5 h. Treatment of 125I-IL-1-labelled IL-1 receptors in Raji and EL4 cells with neuraminidase decreased their molecular mass by approx. Cycloheximide 86-99 interleukin 1 alpha Homo sapiens 25-29 2470302-1 1988 Keratinocytes in culture produce detectable amounts of IL-1 alpha mRNA constitutively and can be stimulated to express increased amounts of IL-1 alpha mRNA by cycloheximide, PMA, and retinoic acid. Cycloheximide 159-172 interleukin 1 alpha Homo sapiens 55-65 3148377-10 1988 Furthermore, the partial maintenance of LPS-induced IL-1 production seen after cells were pre-incubated in gamma-IFN was markedly increased by the inclusion of 0.25 microgram/ml cycloheximide during the 24 h pre-incubation. Cycloheximide 178-191 interleukin 1 alpha Homo sapiens 52-56 3148377-12 1988 Pre-incubation in gamma-IFN and cycloheximide leads to separate but synergistic effects on the maintenance of LPS-induced IL-1 production in cultured monocytes. Cycloheximide 32-45 interleukin 1 alpha Homo sapiens 122-126 3262700-7 1988 The inhibitory action of IL1 on poly(I).poly(C)-induced IFN-beta synthesis was abolished in the presence of cycloheximide, suggesting that it is mediated indirectly by an IL1-induced product in the FS-4 cells. Cycloheximide 108-121 interleukin 1 alpha Homo sapiens 25-28 3262700-7 1988 The inhibitory action of IL1 on poly(I).poly(C)-induced IFN-beta synthesis was abolished in the presence of cycloheximide, suggesting that it is mediated indirectly by an IL1-induced product in the FS-4 cells. Cycloheximide 108-121 interleukin 1 alpha Homo sapiens 171-174 3276786-6 1988 The enhancing effect of IL-1 alpha on IFN-beta 2 gene transcription, but not that of TNF, PDGF, or IFN-beta 1, is inhibited by cycloheximide, suggesting that newly-synthesized protein is involved in the increase in IFN-beta 2 transcription in response to IL-1 alpha but not in the response to the other stimuli. Cycloheximide 127-140 interleukin 1 alpha Homo sapiens 24-34 3276786-6 1988 The enhancing effect of IL-1 alpha on IFN-beta 2 gene transcription, but not that of TNF, PDGF, or IFN-beta 1, is inhibited by cycloheximide, suggesting that newly-synthesized protein is involved in the increase in IFN-beta 2 transcription in response to IL-1 alpha but not in the response to the other stimuli. Cycloheximide 127-140 interleukin 1 alpha Homo sapiens 255-265 2527510-4 1989 The steady-state level of IL-1 alpha mRNA in these cells could be drastically increased by a short culture of the cells with the protein synthesis inhibitor cycloheximide or with PMA. Cycloheximide 157-170 interleukin 1 alpha Homo sapiens 26-36 3260778-5 1988 Chondrocytes incubated with cycloheximide showed a first-order decrease in rate of uptake of radiolabelled sulphate (t1/2 = 25 mins) but interleukin 1 induced inhibition showed a delay of at least 1 hr, consistent with a requirement to deplete intracellular pools of protein before effects on post-translational events could be observed. Cycloheximide 28-41 interleukin 1 alpha Homo sapiens 137-150 2470302-0 1988 Interleukin-1 alpha mRNA induced by cycloheximide PMA, and retinoic acid is reduced by dexamethasone in PAM-212 keratinocytes. Cycloheximide 36-49 interleukin 1 alpha Homo sapiens 0-19 2470302-1 1988 Keratinocytes in culture produce detectable amounts of IL-1 alpha mRNA constitutively and can be stimulated to express increased amounts of IL-1 alpha mRNA by cycloheximide, PMA, and retinoic acid. Cycloheximide 159-172 interleukin 1 alpha Homo sapiens 140-150 3121313-6 1987 Cycloheximide even superinduces this gene when added together with poly(rI).poly(rC) and interleukin-1 (but not when added with interferon). Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 89-102 3278078-9 1988 Cycloheximide at 5-10 micrograms/ml completely blocked IL-1-induced breakdown. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 55-59 2890635-8 1987 The induction of SAA is pretranslational and is likely to be mediated by protein factor(s) since incubation with cycloheximide diminished IL-1-dependent increase in SAA mRNA. Cycloheximide 113-126 interleukin 1 alpha Homo sapiens 138-142 3495577-5 1987 Cycloheximide inhibition of new protein synthesis causes a superinduction of IL 1 message, but does not alter the initial kinetics of message production. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 77-81 3497983-5 1987 rIL-1 induced IL-1-alpha mRNA only in EC treated concomitantly with cycloheximide (2 micrograms/ml). Cycloheximide 68-81 interleukin 1 alpha Homo sapiens 14-24 3494807-6 1987 IL-1 alpha mRNA was detected in SMC treated with cycloheximide (1 microgram/ml) and rIL-1 beta, or cycloheximide alone. Cycloheximide 49-62 interleukin 1 alpha Homo sapiens 0-10 3494807-6 1987 IL-1 alpha mRNA was detected in SMC treated with cycloheximide (1 microgram/ml) and rIL-1 beta, or cycloheximide alone. Cycloheximide 99-112 interleukin 1 alpha Homo sapiens 0-10 3526909-4 1986 IL-1 alpha mRNA was also detected when endothelial cells were exposed to endotoxin under "superinduction" conditions in the presence of cycloheximide. Cycloheximide 136-149 interleukin 1 alpha Homo sapiens 0-10 3545852-3 1987 Combined treatment with cycloheximide and actinomycin D also stimulates production and enhances production induced by IL 1 or poly(rI).poly(rC). Cycloheximide 24-37 interleukin 1 alpha Homo sapiens 118-122 3491091-7 1986 Interleukin-1 alpha mRNA was detected when SMC were incubated with endotoxin under "superinduction" conditions with cycloheximide. Cycloheximide 116-129 interleukin 1 alpha Homo sapiens 0-19 3877078-7 1985 IL-1 induction of endothelial adhesivity was concentration dependent (maximum, 10 U/ml), time dependent (peak, 4-6 h), and reversible, was blocked by cycloheximide (10 micrograms/ml) or actinomycin D (5 micrograms/ml) but not by acetylsalicylic acid (100 microM), and occurred without detectable endothelial cell damage. Cycloheximide 150-163 interleukin 1 alpha Homo sapiens 0-4 2416819-8 1986 A protein synthesis inhibitor (cycloheximide) and an RNA synthesis inhibitor (actinomycin D) prevented the acquisition of adhesiveness stimulated by IL 1 and endotoxin but not by TPA. Cycloheximide 31-44 interleukin 1 alpha Homo sapiens 149-153 3878084-6 1985 Cycloheximide and actinomycin D block these IL-1 actions on endothelium, which suggests the requirement for de novo protein synthesis. Cycloheximide 0-13 interleukin 1 alpha Homo sapiens 44-48 2993420-6 1985 The enhanced binding and cytotoxicity of IL 1-treated target cells was only observed when the latter cells were preincubated with IL 1 at 37 degrees C, and was not evident at 4 degrees C. Furthermore, the IL 1-mediated effect could be abolished by treating the target cells with cycloheximide before the IL 1 pulse, or by adding rabbit anti-human IL 1 together with the IL 1. Cycloheximide 279-292 interleukin 1 alpha Homo sapiens 130-134 2993420-6 1985 The enhanced binding and cytotoxicity of IL 1-treated target cells was only observed when the latter cells were preincubated with IL 1 at 37 degrees C, and was not evident at 4 degrees C. Furthermore, the IL 1-mediated effect could be abolished by treating the target cells with cycloheximide before the IL 1 pulse, or by adding rabbit anti-human IL 1 together with the IL 1. Cycloheximide 279-292 interleukin 1 alpha Homo sapiens 41-45 2993420-6 1985 The enhanced binding and cytotoxicity of IL 1-treated target cells was only observed when the latter cells were preincubated with IL 1 at 37 degrees C, and was not evident at 4 degrees C. Furthermore, the IL 1-mediated effect could be abolished by treating the target cells with cycloheximide before the IL 1 pulse, or by adding rabbit anti-human IL 1 together with the IL 1. Cycloheximide 279-292 interleukin 1 alpha Homo sapiens 130-134 3876401-7 1985 Addition of cycloheximide blocked generation of IL-1 activity. Cycloheximide 12-25 interleukin 1 alpha Homo sapiens 48-52 2993420-6 1985 The enhanced binding and cytotoxicity of IL 1-treated target cells was only observed when the latter cells were preincubated with IL 1 at 37 degrees C, and was not evident at 4 degrees C. Furthermore, the IL 1-mediated effect could be abolished by treating the target cells with cycloheximide before the IL 1 pulse, or by adding rabbit anti-human IL 1 together with the IL 1. Cycloheximide 279-292 interleukin 1 alpha Homo sapiens 130-134 2993420-6 1985 The enhanced binding and cytotoxicity of IL 1-treated target cells was only observed when the latter cells were preincubated with IL 1 at 37 degrees C, and was not evident at 4 degrees C. Furthermore, the IL 1-mediated effect could be abolished by treating the target cells with cycloheximide before the IL 1 pulse, or by adding rabbit anti-human IL 1 together with the IL 1. Cycloheximide 279-292 interleukin 1 alpha Homo sapiens 130-134 2993420-6 1985 The enhanced binding and cytotoxicity of IL 1-treated target cells was only observed when the latter cells were preincubated with IL 1 at 37 degrees C, and was not evident at 4 degrees C. Furthermore, the IL 1-mediated effect could be abolished by treating the target cells with cycloheximide before the IL 1 pulse, or by adding rabbit anti-human IL 1 together with the IL 1. Cycloheximide 279-292 interleukin 1 alpha Homo sapiens 130-134