PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9832332-6 1998 Inhibition of protein synthesis (with cycloheximide) raised basal GMCSF mRNA transcripts to detectable levels, augmented IL-1-induced increases in GMCSF mRNA levels, and exhibited negative regulation by cAMP. Cycloheximide 38-51 colony stimulating factor 2 Homo sapiens 66-71 9562439-4 1998 This increase in GM-CSF mRNA levels in response to shear stress depended on protein synthesis, because it was blocked by cycloheximide. Cycloheximide 121-134 colony stimulating factor 2 Homo sapiens 17-23 9832332-6 1998 Inhibition of protein synthesis (with cycloheximide) raised basal GMCSF mRNA transcripts to detectable levels, augmented IL-1-induced increases in GMCSF mRNA levels, and exhibited negative regulation by cAMP. Cycloheximide 38-51 colony stimulating factor 2 Homo sapiens 147-152 7829234-7 1995 The protein synthesis inhibitor cycloheximide super-induced basal and GM-CSF-induced ICAM-I transcripts, thus excluding a role for secondary polypeptide mediators. Cycloheximide 32-45 colony stimulating factor 2 Homo sapiens 70-76 8874185-4 1996 Translational inhibition by cycloheximide (CHX) significantly increased GM-CSF mRNA accumulation and half-life by three-fold in activated cord MNC, but had a minimal effect in activated adult MNC as compared with PMA + PHA alone. Cycloheximide 28-41 colony stimulating factor 2 Homo sapiens 72-78 8874185-4 1996 Translational inhibition by cycloheximide (CHX) significantly increased GM-CSF mRNA accumulation and half-life by three-fold in activated cord MNC, but had a minimal effect in activated adult MNC as compared with PMA + PHA alone. Cycloheximide 43-46 colony stimulating factor 2 Homo sapiens 72-78 8562392-4 1996 Cycloheximide abrogated the effects of both GM-CSF and butyrate. Cycloheximide 0-13 colony stimulating factor 2 Homo sapiens 44-50 9051287-6 1997 The release of GM-CSF elicited by the cytokine mixture was inhibited by cycloheximide and dexamethasone. Cycloheximide 72-85 colony stimulating factor 2 Homo sapiens 15-21 8786314-4 1996 Enhanced LT synthesis required a minimum of 6 h of GM-CSF pretreatment, suggesting that protein synthesis was required for enhanced LT production; indeed, cycloheximide completely abolished the GM-CSF effect on LT synthesis. Cycloheximide 155-168 colony stimulating factor 2 Homo sapiens 194-200 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 colony stimulating factor 2 Homo sapiens 58-64 7540853-6 1995 The simultaneous addition, to deprived cells, of the growth factor, and of cycloheximide (CHX) for 2 h inhibited GM-CSF mRNA expression, suggesting the requirement for newly made proteins for GM-CSF gene transcription. Cycloheximide 75-88 colony stimulating factor 2 Homo sapiens 113-119 7540853-6 1995 The simultaneous addition, to deprived cells, of the growth factor, and of cycloheximide (CHX) for 2 h inhibited GM-CSF mRNA expression, suggesting the requirement for newly made proteins for GM-CSF gene transcription. Cycloheximide 75-88 colony stimulating factor 2 Homo sapiens 192-198 7540853-6 1995 The simultaneous addition, to deprived cells, of the growth factor, and of cycloheximide (CHX) for 2 h inhibited GM-CSF mRNA expression, suggesting the requirement for newly made proteins for GM-CSF gene transcription. Cycloheximide 90-93 colony stimulating factor 2 Homo sapiens 113-119 7540853-6 1995 The simultaneous addition, to deprived cells, of the growth factor, and of cycloheximide (CHX) for 2 h inhibited GM-CSF mRNA expression, suggesting the requirement for newly made proteins for GM-CSF gene transcription. Cycloheximide 90-93 colony stimulating factor 2 Homo sapiens 192-198 7780040-6 1995 In contrast, the known translational inhibitor cycloheximide did not demonstrate selectivity for IL-6; this agent decreased the GM-CSF-induced increase in total translational activity in parallel with its effects on IL-6. Cycloheximide 47-60 colony stimulating factor 2 Homo sapiens 128-134 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 colony stimulating factor 2 Homo sapiens 327-333 7795173-8 1995 The CSF release was dependent on protein synthesis as it was completely inhibited by cycloheximide (50.0 micrograms/ml). Cycloheximide 85-98 colony stimulating factor 2 Homo sapiens 4-7 1280481-4 1992 Inhibition of RNA and protein synthesis by actinomycin-D and cycloheximide impeded the protection of apoptosis by GM-CSF. Cycloheximide 61-74 colony stimulating factor 2 Homo sapiens 114-120 8145039-6 1994 The stimulatory effect of GM-CSF on FLAP mRNA was inhibited by prior treatment of the cells with the transcription inhibitor, actinomycin D, and pretreatment of the cells with the protein synthesis inhibitor, cycloheximide, failed to prevent the increase in FLAP mRNA induced by GM-CSF. Cycloheximide 209-222 colony stimulating factor 2 Homo sapiens 26-32 8481893-4 1993 In contrast, receptor increase after 18 h of incubation with insulin and GM-CSF was sensitive to cycloheximide indicating that long term effects of these growth factors are mediated through protein synthesis. Cycloheximide 97-110 colony stimulating factor 2 Homo sapiens 73-79 8283055-5 1994 Prior treatment of the cells with the protein synthesis inhibitor cycloheximide abolished this effect of GM-CSF. Cycloheximide 66-79 colony stimulating factor 2 Homo sapiens 105-111 8262555-9 1993 Cycloheximide (10(-6) M) significantly inhibited GM-CSF-induced CD69 expression, suggesting a requirement for protein synthesis. Cycloheximide 0-13 colony stimulating factor 2 Homo sapiens 49-55 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 colony stimulating factor 2 Homo sapiens 97-103 8358016-3 1993 A close correlation was observed between the priming kinetics of GM-CSF on 5-LO activation and on LT synthesis; moreover, the effects of the cytokine on both 5-LO activation and LT synthesis were inhibited when the cells had been exposed to either the protein synthesis inhibitor, cycloheximide (CX), or the transcription inhibitor, actinomycin D (AD), prior to incubation with GM-CSF. Cycloheximide 281-294 colony stimulating factor 2 Homo sapiens 65-71 8358016-3 1993 A close correlation was observed between the priming kinetics of GM-CSF on 5-LO activation and on LT synthesis; moreover, the effects of the cytokine on both 5-LO activation and LT synthesis were inhibited when the cells had been exposed to either the protein synthesis inhibitor, cycloheximide (CX), or the transcription inhibitor, actinomycin D (AD), prior to incubation with GM-CSF. Cycloheximide 296-298 colony stimulating factor 2 Homo sapiens 65-71 2064996-7 1991 Inhibition of protein synthesis with cycloheximide also had no detectable effect on EGR-1 gene transcription but was associated with superinduction of EGR-1 mRNA levels in GM-CSF-treated cells. Cycloheximide 37-50 colony stimulating factor 2 Homo sapiens 172-178 1633112-6 1992 Run-on analysis showed that transcription of the GM-CSF gene was low to undetectable in unstimulated cells; stimulation led to transcriptional activation, which was weak at 6 h but had increased 16-fold at 24 h. In addition, the mRNA half-life decreased during activation, from 2.5 h at 6 h down to 45 min at 24 h. Cycloheximide treatment increased GM-CSF mRNA half-life (3- and 4-fold, respectively). Cycloheximide 315-328 colony stimulating factor 2 Homo sapiens 49-55 1714478-4 1991 Increased levels of the CSF Ag were detected after 2 to 8 h stimulation with IL-1, and the optimum dose of IL-1 was 10 to 100 U/ml (0.06 to 0.6 nM IL-1 alpha; 0.02 to 0.2 nM IL-1 beta); neither CSF was detectable in nonstimulated cultures nor in IL-1-stimulated cultures treated with actinomycin D or cycloheximide, indicating the requirement for de novo RNA and protein synthesis. Cycloheximide 301-314 colony stimulating factor 2 Homo sapiens 24-27 1903413-5 1991 Treatment of monocytes with cycloheximide in the presence of GM-CSF blocked TOMS-1Ag induction completely, indicating that de novo protein synthesis was required for its expression. Cycloheximide 28-41 colony stimulating factor 2 Homo sapiens 61-67 2674950-3 1989 GM-CSF-stimulated adherence must require new RNA and protein synthesis because actinomycin D and cycloheximide abolished existing adherence and prevented further monocyte attachment. Cycloheximide 97-110 colony stimulating factor 2 Homo sapiens 0-6 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 colony stimulating factor 2 Homo sapiens 118-124 12648514-6 2003 Cycloheximide prevented protection, indicating that GM-CSF might induce synthesis of antiapoptotic proteins. Cycloheximide 0-13 colony stimulating factor 2 Homo sapiens 52-58 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 colony stimulating factor 2 Homo sapiens 77-83 2463477-5 1988 Both G- and GM-CSF mRNA concentrations coordinately increased after exposure of the cells to TNF alpha (greater than or equal to 5 ng/ml), 12-O-tetradecanoylphorbol 13-acetate (TPA) (greater than or equal to 5 x 10(-10) M), or cycloheximide (20 micrograms/ml). Cycloheximide 227-240 colony stimulating factor 2 Homo sapiens 12-18 3290254-4 1988 Studies using cycloheximide as a protein synthesis inhibitor showed that the inhibitory action of 1,25(OH)2D3 on GM-CSF expression was dependent on new protein synthesis. Cycloheximide 14-27 colony stimulating factor 2 Homo sapiens 113-119