PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21749909-4 2011 Co-treatment of MM6 cells with IFN-gamma and cycloheximide caused a superinduction of SECTM1 mRNA expression while cycloheximide alone had no effect, illustrating that de novo protein synthesis is not required for IFN-gamma enhanced expression of SECTM1 mRNA, a characteristic of IFN early response genes. Cycloheximide 115-128 interferon alpha 1 Homo sapiens 31-34 15919906-8 2005 The stimulation of IRF-7 gene expression by IFN-alpha in glial cell culture was prevented by cycloheximide. Cycloheximide 93-106 interferon alpha 1 Homo sapiens 44-53 15937643-4 2005 IFN-induced TP mRNA accumulation was not inhibited by the protein synthesis inhibitor cycloheximide, but was strongly blocked by the transcription inhibitor actinomycin D, as well as by transcription factor decoy oligodeoxynucleotides containing the putative IFN response element or the gamma-activated sequence in the TP promoter. Cycloheximide 86-99 interferon alpha 1 Homo sapiens 0-3 14697509-5 2004 Analysis of expression difference between them and IFN signal factors, CaSTAT1 and CaIRF7, indicated that their transcriptions were mediated possibly through JAK-STAT signal pathway, which was further supported by the induction analysis in UV-inactivated GCHV infected, IFN-treated and untreated cells in the presence or absence of cycloheximide (CHX), a potent inhibitor of protein synthesis. Cycloheximide 332-345 interferon alpha 1 Homo sapiens 51-54 14697509-5 2004 Analysis of expression difference between them and IFN signal factors, CaSTAT1 and CaIRF7, indicated that their transcriptions were mediated possibly through JAK-STAT signal pathway, which was further supported by the induction analysis in UV-inactivated GCHV infected, IFN-treated and untreated cells in the presence or absence of cycloheximide (CHX), a potent inhibitor of protein synthesis. Cycloheximide 332-345 interferon alpha 1 Homo sapiens 270-273 14697509-5 2004 Analysis of expression difference between them and IFN signal factors, CaSTAT1 and CaIRF7, indicated that their transcriptions were mediated possibly through JAK-STAT signal pathway, which was further supported by the induction analysis in UV-inactivated GCHV infected, IFN-treated and untreated cells in the presence or absence of cycloheximide (CHX), a potent inhibitor of protein synthesis. Cycloheximide 347-350 interferon alpha 1 Homo sapiens 51-54 14697509-5 2004 Analysis of expression difference between them and IFN signal factors, CaSTAT1 and CaIRF7, indicated that their transcriptions were mediated possibly through JAK-STAT signal pathway, which was further supported by the induction analysis in UV-inactivated GCHV infected, IFN-treated and untreated cells in the presence or absence of cycloheximide (CHX), a potent inhibitor of protein synthesis. Cycloheximide 347-350 interferon alpha 1 Homo sapiens 270-273 12070711-4 2002 Cycloheximide, a protein synthesis inhibitor, also induced uPAR mRNA accumulation either alone or in combination with IFN-alpha or IFN-gamma, suggesting that the effect on uPAR mRNA levels activated by IFN-alpha or IFN-gamma does not require de novo protein synthesis. Cycloheximide 0-13 interferon alpha 1 Homo sapiens 118-127 12070711-4 2002 Cycloheximide, a protein synthesis inhibitor, also induced uPAR mRNA accumulation either alone or in combination with IFN-alpha or IFN-gamma, suggesting that the effect on uPAR mRNA levels activated by IFN-alpha or IFN-gamma does not require de novo protein synthesis. Cycloheximide 0-13 interferon alpha 1 Homo sapiens 202-211 9712367-2 1998 The time courses of the inhibition of IFN-gamma-induced kynurenine synthesis by actinomycin D and cycloheximide showed that the indoleamine dioxygenase gene was transcribed as early as 2 h and translated as early as 5 h after initiation of IFN treatment. Cycloheximide 98-111 interferon alpha 1 Homo sapiens 38-41 11444904-7 2001 Cycloheximide treatment diminished the effect of proteasome inhibitors on ISG induction, implicating an IFN/dsRNA-induced protein in this activity. Cycloheximide 0-13 interferon alpha 1 Homo sapiens 104-107 1310814-3 1992 In the presence of the protein synthesis inhibitor cycloheximide (CHX), the frequency of IFN-alpha mRNA-containing cells, measured after 6h, was decreased by 85-90%. Cycloheximide 51-64 interferon alpha 1 Homo sapiens 89-98 8427967-5 1993 Spectrin reorganization induced by IFN-alpha was abrogated by the protein synthesis inhibitor cycloheximide. Cycloheximide 94-107 interferon alpha 1 Homo sapiens 35-44 1316484-5 1992 In contrast, cycloheximide treatment increased stable mRNA levels and transcription initiation rates from both the IE94-IFN and IE94-CAT hybrid genes. Cycloheximide 13-26 interferon alpha 1 Homo sapiens 120-123 9268319-7 1997 Continuous presence of IFN-alpha was necessary for maintaining prolonged activation of ISGF3 and of Janus kinases, an activity that was blocked by antibodies to IFN-alpha or by cycloheximide. Cycloheximide 177-190 interferon alpha 1 Homo sapiens 23-32 8914344-9 1996 Following exposure of cells to combinations of drugs and IFN alpha, the percentage inhibition for Class I and ICAM-1 in the case of SKV14 and 5367 lines in the presence of cycloheximide (10 micrograms/mL) were 82%, 85% and 57%, 45% respectively. Cycloheximide 172-185 interferon alpha 1 Homo sapiens 57-66 8142954-2 1994 We found that protein synthesis inhibition by cycloheximide (CHX) blocked IFN alpha-mRNA expression, except when PBMC were preincubated with a conditioned medium as a potential source of cytokines. Cycloheximide 46-59 interferon alpha 1 Homo sapiens 74-83 8142954-2 1994 We found that protein synthesis inhibition by cycloheximide (CHX) blocked IFN alpha-mRNA expression, except when PBMC were preincubated with a conditioned medium as a potential source of cytokines. Cycloheximide 61-64 interferon alpha 1 Homo sapiens 74-83 1310814-3 1992 In the presence of the protein synthesis inhibitor cycloheximide (CHX), the frequency of IFN-alpha mRNA-containing cells, measured after 6h, was decreased by 85-90%. Cycloheximide 66-69 interferon alpha 1 Homo sapiens 89-98 1734947-11 1992 Moreover, cycloheximide treatment abolished the protective effect against NK-CMC induced by IFN-alpha or by IL-2. Cycloheximide 10-23 interferon alpha 1 Homo sapiens 92-101 1666118-2 1991 The protein synthesis inhibitor cycloheximide (CHX) totally prevented the appearance of both IFN-alpha and IFN-beta mRNA, also in cultures supplemented with a conditioned medium (CM) assumed to contain soluble factors necessary for the IFN induction. Cycloheximide 32-45 interferon alpha 1 Homo sapiens 93-102 1666118-2 1991 The protein synthesis inhibitor cycloheximide (CHX) totally prevented the appearance of both IFN-alpha and IFN-beta mRNA, also in cultures supplemented with a conditioned medium (CM) assumed to contain soluble factors necessary for the IFN induction. Cycloheximide 32-45 interferon alpha 1 Homo sapiens 93-96 1666118-2 1991 The protein synthesis inhibitor cycloheximide (CHX) totally prevented the appearance of both IFN-alpha and IFN-beta mRNA, also in cultures supplemented with a conditioned medium (CM) assumed to contain soluble factors necessary for the IFN induction. Cycloheximide 47-50 interferon alpha 1 Homo sapiens 93-102 1666118-2 1991 The protein synthesis inhibitor cycloheximide (CHX) totally prevented the appearance of both IFN-alpha and IFN-beta mRNA, also in cultures supplemented with a conditioned medium (CM) assumed to contain soluble factors necessary for the IFN induction. Cycloheximide 47-50 interferon alpha 1 Homo sapiens 93-96 2048200-5 1991 Inhibition of protein synthesis with cycloheximide during IFN-alpha or CsA treatment blocked their ability to reduce the expression of c-myc. Cycloheximide 37-50 interferon alpha 1 Homo sapiens 58-67 2555698-3 1989 Activation by IFN-alpha was rapid, transient, and cycloheximide resistant. Cycloheximide 50-63 interferon alpha 1 Homo sapiens 14-23 34960758-3 2021 RESULTS: While IFNs alone were insufficient to completely abolish replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), IFNalpha, in combination with remdesivir, EIDD-2801, camostat, cycloheximide, or convalescent serum, proved to be more effective. Cycloheximide 206-219 interferon alpha 1 Homo sapiens 143-151 2127700-8 1990 In both naive and TPA-desensitized human fibroblasts or WISH cells, prolonged IFN treatment induced a desensitized state that was reversible by cycloheximide. Cycloheximide 144-157 interferon alpha 1 Homo sapiens 78-81 2516865-3 1989 Using a combined treatment with cycloheximide and actinomycin D we observed that in HeLa cells IFN-alpha did not need ongoing protein synthesis to induce the enzyme, whereas the addition of cycloheximide prevented the induction by IFN-gamma. Cycloheximide 32-45 interferon alpha 1 Homo sapiens 95-104 2452894-8 1988 When cells are treated with IFN-alpha or IFN-gamma in the presence of cycloheximide, and actinomycin D is added prior to the removal of the cycloheximide, the cells produce the IFN-induced 56,000-dalton protein and develop an antiviral state in response to both IFN-alpha and IFN-gamma. Cycloheximide 70-83 interferon alpha 1 Homo sapiens 28-37 2464596-4 1989 The actions of phorbol esters are only seen in those types of cultured cells where cycloheximide in the presence of IFN prevents long term IFN treatment of cells from inducing a "desensitized state." Cycloheximide 83-96 interferon alpha 1 Homo sapiens 139-142 2469744-4 1989 Cycloheximide combined with chloramphenicol further inhibited the antiviral effect of IFN than that observed by either drug alone. Cycloheximide 0-13 interferon alpha 1 Homo sapiens 86-89 2452894-8 1988 When cells are treated with IFN-alpha or IFN-gamma in the presence of cycloheximide, and actinomycin D is added prior to the removal of the cycloheximide, the cells produce the IFN-induced 56,000-dalton protein and develop an antiviral state in response to both IFN-alpha and IFN-gamma. Cycloheximide 70-83 interferon alpha 1 Homo sapiens 28-31 2452894-8 1988 When cells are treated with IFN-alpha or IFN-gamma in the presence of cycloheximide, and actinomycin D is added prior to the removal of the cycloheximide, the cells produce the IFN-induced 56,000-dalton protein and develop an antiviral state in response to both IFN-alpha and IFN-gamma. Cycloheximide 70-83 interferon alpha 1 Homo sapiens 262-271 2452894-8 1988 When cells are treated with IFN-alpha or IFN-gamma in the presence of cycloheximide, and actinomycin D is added prior to the removal of the cycloheximide, the cells produce the IFN-induced 56,000-dalton protein and develop an antiviral state in response to both IFN-alpha and IFN-gamma. Cycloheximide 140-153 interferon alpha 1 Homo sapiens 28-37 2452894-8 1988 When cells are treated with IFN-alpha or IFN-gamma in the presence of cycloheximide, and actinomycin D is added prior to the removal of the cycloheximide, the cells produce the IFN-induced 56,000-dalton protein and develop an antiviral state in response to both IFN-alpha and IFN-gamma. Cycloheximide 140-153 interferon alpha 1 Homo sapiens 28-31 2452894-8 1988 When cells are treated with IFN-alpha or IFN-gamma in the presence of cycloheximide, and actinomycin D is added prior to the removal of the cycloheximide, the cells produce the IFN-induced 56,000-dalton protein and develop an antiviral state in response to both IFN-alpha and IFN-gamma. Cycloheximide 140-153 interferon alpha 1 Homo sapiens 262-271 6818330-6 1982 Hydrocortisone also blocked the induction of IFN by double-stranded RNA (dsRNA), cycloheximide and actinomycin D in FS11 cells. Cycloheximide 81-94 interferon alpha 1 Homo sapiens 45-48 3312425-5 1987 The IFN effect was not expressed at 4 degrees C, and the ribosomal 60S subunit inactivators, cycloheximide, abrin, and shigella toxin, completely blocked the expression of the IFN-induced anti-invasive state of the cell. Cycloheximide 93-106 interferon alpha 1 Homo sapiens 176-179 2433469-7 1987 Cycloheximide treatment (without virus infection) also gave a rapid 30-fold increase in steady-state levels of correctly initiated mRNA from both types of IE94-IFN hybrid genes, but had no effect on cells containing the IE175-IFN construct. Cycloheximide 0-13 interferon alpha 1 Homo sapiens 160-163 2433469-7 1987 Cycloheximide treatment (without virus infection) also gave a rapid 30-fold increase in steady-state levels of correctly initiated mRNA from both types of IE94-IFN hybrid genes, but had no effect on cells containing the IE175-IFN construct. Cycloheximide 0-13 interferon alpha 1 Homo sapiens 226-229 3027204-5 1986 However, the presence of cycloheximide during incubation with IFN had no effect on the synthesis of CKp76 after removal of both agents. Cycloheximide 25-38 interferon alpha 1 Homo sapiens 62-65 3097508-8 1986 This rapid turnover could be blocked by actinomycin D or cycloheximide indicating that another IFN-inducible protein may mediate this process. Cycloheximide 57-70 interferon alpha 1 Homo sapiens 95-98 2478164-4 1987 However, when cycloheximide, an inhibitor of protein synthesis is added at the time of virus infection, extensive cleavage or rRNA is observed in IFN-treated, infected cells. Cycloheximide 14-27 interferon alpha 1 Homo sapiens 146-149 3007667-3 1986 Experiments using cycloheximide or actinomycin D and kinetic studies showed that this IFN originated mainly in IFN which resided within the cell as a result of the first induction and was released after the second stimulation. Cycloheximide 18-31 interferon alpha 1 Homo sapiens 86-89 3007667-3 1986 Experiments using cycloheximide or actinomycin D and kinetic studies showed that this IFN originated mainly in IFN which resided within the cell as a result of the first induction and was released after the second stimulation. Cycloheximide 18-31 interferon alpha 1 Homo sapiens 111-114 3773893-6 1986 If IFN priming is carried out in the presence of cycloheximide, a approximately 200-fold increase in induction is observed. Cycloheximide 49-62 interferon alpha 1 Homo sapiens 3-6 6091048-3 1984 The IFN-beta 1 RNA synthesized by nuclei of uninduced SR117-21E cells is similar to that made by nuclei of poly(rI):(rC)-induced cells, but does not accumulate and hence no IFN is produced unless the cells have been treated either by ds RNA or by cycloheximide. Cycloheximide 247-260 interferon alpha 1 Homo sapiens 4-7 6319493-10 1984 Cycloheximide, puromycin, emetine, and actinomycin D blocked NK activation by IFN and poly I:C as well as the acquisition of resistance to PGE2-mediated suppression. Cycloheximide 0-13 interferon alpha 1 Homo sapiens 78-81 6198116-8 1984 Cycloheximide has been shown to inhibit the stimulatory effect of IFN on human and murine NK cells whilst not influencing endogenous cytotoxicity. Cycloheximide 0-13 interferon alpha 1 Homo sapiens 66-69 6198116-9 1984 In contrast, we found that both the stimulatory effect of IFN on rat NK cells and endogenous activity were equally inhibited by cycloheximide. Cycloheximide 128-141 interferon alpha 1 Homo sapiens 58-61 6099864-4 1984 IFN was inhibited by treatment of cells with either actinomycin D or cycloheximide, indicating the requirement of IFN-mRNA and protein for de novo synthesis. Cycloheximide 69-82 interferon alpha 1 Homo sapiens 0-3 6306284-4 1983 In contrast, cycloheximide without double-stranded RNA could induce significant levels of human IFN in the bovine papillomavirus IFN-beta 1 mouse transformants. Cycloheximide 13-26 interferon alpha 1 Homo sapiens 96-99 6306284-4 1983 In contrast, cycloheximide without double-stranded RNA could induce significant levels of human IFN in the bovine papillomavirus IFN-beta 1 mouse transformants. Cycloheximide 13-26 interferon alpha 1 Homo sapiens 129-132 6306284-5 1983 After cycloheximide treatment, these cells contained IFN-beta 1 mRNA whose 5" ends originated in the authentic start site of the human IFN-beta 1 gene, as shown by S1 nuclease mapping. Cycloheximide 6-19 interferon alpha 1 Homo sapiens 53-56 6306284-5 1983 After cycloheximide treatment, these cells contained IFN-beta 1 mRNA whose 5" ends originated in the authentic start site of the human IFN-beta 1 gene, as shown by S1 nuclease mapping. Cycloheximide 6-19 interferon alpha 1 Homo sapiens 135-138 6306284-7 1983 The results also confirmed that the inhibitor of protein synthesis, cycloheximide, can induce expression of a human IFN gene. Cycloheximide 68-81 interferon alpha 1 Homo sapiens 116-119 7149923-1 1982 The effect of cycloheximide, chloramphenicol, ethidium bromide (EB), aurin tricarboxylic acid (ATA), and actinomycin D on the production of interferon (IFN) in human embryo fibroblasts (HAT) and L929 cells, stimulated with RNA from Piptoporus betulinus (Pb-RNA) was studied. Cycloheximide 14-27 interferon alpha 1 Homo sapiens 140-156 7149923-2 1982 Treatment of HAT cells with cycloheximide superinduced the production of IFN. Cycloheximide 28-41 interferon alpha 1 Homo sapiens 73-76