PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9886918-8 1999 Exposure to 25 nM thrombin for >60 min prevented rapid cycloheximide-insensitive PAR-1 reappearance. Cycloheximide 58-71 coagulation factor II, thrombin Homo sapiens 18-26 16293985-4 2005 In these cells, we further show that thrombin-induced VEGF secretion was blocked by cycloheximide and actinomycin D, indicating that de novo protein synthesis is essential for this process. Cycloheximide 84-97 coagulation factor II, thrombin Homo sapiens 37-45 12181122-3 2002 Thrombin stimulated the accumulation of HSP27 dose dependently between 0.01 and 1 U/ml and cycloheximide reduced the accumulation. Cycloheximide 91-104 coagulation factor II, thrombin Homo sapiens 0-8 10749718-5 2000 Surprisingly, inhibition of E-selectin expression with the general protein synthesis inhibitor cycloheximide induced P-selectin expression 4 h after thrombin stimulation. Cycloheximide 95-108 coagulation factor II, thrombin Homo sapiens 149-157 10749718-6 2000 Cycloheximide and thrombin (4 h) induced sufficient P-selectin-dependent rolling to recruit as many neutrophils as were recruited with 4 h of stimulation with thrombin alone. Cycloheximide 0-13 coagulation factor II, thrombin Homo sapiens 159-167 10749718-8 2000 Treatment of endothelium with tumor necrosis factor-alpha (an E-selectin inducer) and cycloheximide also eliminated E-selectin expression but, much like thrombin, induced P-selectin expression and neutrophil recruitment. Cycloheximide 86-99 coagulation factor II, thrombin Homo sapiens 153-161 9886918-9 1999 Cycloheximide-sensitive recovery of cell surface PAR-1 expression required 18 h. Therefore, both duration and concentration of thrombin exposure regulate the time course of recovery of HPAEC surface PAR-1 expression. Cycloheximide 0-13 coagulation factor II, thrombin Homo sapiens 127-135 8611404-5 1996 The enhanced adhesion was significantly inhibited by complexing of thrombin with its inhibitor hirudin, or by serine proteinase inhibition with 3,4-DCI, but was unaffected by pretreatment of tumour cells with actinomycin D or cycloheximide. Cycloheximide 226-239 coagulation factor II, thrombin Homo sapiens 67-75 9820166-4 1998 Both effects of thrombin and PMA on PCA in SW-480 cells were blocked by pretreatment of cells with cycloheximide or actinomycin D, indicating that the response required de novo protein and RNA synthesis. Cycloheximide 99-112 coagulation factor II, thrombin Homo sapiens 16-24 8952883-5 1996 In the presence of elastin peptides lymphocytes show increased proliferation and increased production of an elastase type serine protease apparently identical to PMN-elastase, inhibited by cycloheximide and by anti-PMN elastase antibodies. Cycloheximide 189-202 coagulation factor II, thrombin Homo sapiens 122-137 9163601-7 1997 Rechallenge with thrombin induced rapid surface re-expression of P-selectin, which was independent of de novo protein synthesis, since cycloheximide did not inhibit re-expression. Cycloheximide 135-148 coagulation factor II, thrombin Homo sapiens 17-25 7762612-3 1995 Inhibition of protein synthesis by cycloheximide (2 micrograms/ml) obviated thrombin"s chemotactic effect. Cycloheximide 35-48 coagulation factor II, thrombin Homo sapiens 76-84 8585010-3 1995 These thrombin effects were inhibited by cycloheximide (CHX), an inhibitor of protein biosynthesis. Cycloheximide 41-54 coagulation factor II, thrombin Homo sapiens 6-14 8585010-3 1995 These thrombin effects were inhibited by cycloheximide (CHX), an inhibitor of protein biosynthesis. Cycloheximide 56-59 coagulation factor II, thrombin Homo sapiens 6-14 8134905-5 1993 The t-PA mRNA expression induced by thrombin was completely blocked by pretreatment of the cells with an inhibitor of translation, cycloheximide (CHX). Cycloheximide 131-144 coagulation factor II, thrombin Homo sapiens 36-44 8134905-5 1993 The t-PA mRNA expression induced by thrombin was completely blocked by pretreatment of the cells with an inhibitor of translation, cycloheximide (CHX). Cycloheximide 146-149 coagulation factor II, thrombin Homo sapiens 36-44 1313426-8 1992 Resensitization of the cell to thrombin following a brief exposure to thrombin required up to 24 h and could be inhibited with cycloheximide. Cycloheximide 127-140 coagulation factor II, thrombin Homo sapiens 31-39 1500822-6 1992 The protein synthesis inhibitor, cycloheximide, which itself markedly stimulates the accumulation of PAI-1, appears to prevent the induction by thrombin, suggesting that thrombin may act by inducing another effector such as interleukin-1. Cycloheximide 33-46 coagulation factor II, thrombin Homo sapiens 144-152 1500822-6 1992 The protein synthesis inhibitor, cycloheximide, which itself markedly stimulates the accumulation of PAI-1, appears to prevent the induction by thrombin, suggesting that thrombin may act by inducing another effector such as interleukin-1. Cycloheximide 33-46 coagulation factor II, thrombin Homo sapiens 170-178 1313426-8 1992 Resensitization of the cell to thrombin following a brief exposure to thrombin required up to 24 h and could be inhibited with cycloheximide. Cycloheximide 127-140 coagulation factor II, thrombin Homo sapiens 70-78 1313426-9 1992 Resensitization to TRP42/55 after exposure to thrombin, or to thrombin after exposure to TRP42/55, on the other hand, was detectable within 30 min and could be inhibited by serine/threonine phosphatase inhibitors, but not by cycloheximide. Cycloheximide 225-238 coagulation factor II, thrombin Homo sapiens 62-70 2215247-5 1990 Thrombin-induced ir-endothelin-1 release also was inhibited completely by 10 micrograms/mL cycloheximide. Cycloheximide 91-104 coagulation factor II, thrombin Homo sapiens 0-8 1721042-10 1991 Cycloheximide treatment, however, inhibited the recovery of perforin and serine protease RNAs. Cycloheximide 0-13 coagulation factor II, thrombin Homo sapiens 73-88 3098881-6 1987 This effect was dependent on a free active site in thrombin and specific protein synthesis (inhibited by cycloheximide and dactinomycin) but unrelated to prostacyclin synthesis (no effect of aspirin or indomethacin). Cycloheximide 105-118 coagulation factor II, thrombin Homo sapiens 51-59 2113968-5 1990 All thrombin effects, however, were suppressed by the simultaneous addition of cycloheximide, indicating that the enhancing effects of thrombin were due to an increase in the production of PAs and PAI-1, via protein synthesis. Cycloheximide 79-92 coagulation factor II, thrombin Homo sapiens 4-12 2113968-5 1990 All thrombin effects, however, were suppressed by the simultaneous addition of cycloheximide, indicating that the enhancing effects of thrombin were due to an increase in the production of PAs and PAI-1, via protein synthesis. Cycloheximide 79-92 coagulation factor II, thrombin Homo sapiens 135-143 2104763-8 1990 However, thrombin did appear to partially protect TC II release from inhibition by cycloheximide. Cycloheximide 83-96 coagulation factor II, thrombin Homo sapiens 9-17 2417348-4 1985 The thrombin-induced thromboplastin activity was inhibited by incubation of the cells with cycloheximide (2 micrograms/ml) or actinomycin D (2 micrograms/ml) showing that the response depended on de novo protein and RNA synthesis. Cycloheximide 91-104 coagulation factor II, thrombin Homo sapiens 4-12 3092394-7 1986 Both the decrease in PGI2 production after thrombin/ionophore and the increase after re-stimulation with AA were blunted in the presence of the protein synthesis inhibitor cycloheximide (0.1-0.2 micrograms/ml). Cycloheximide 172-185 coagulation factor II, thrombin Homo sapiens 43-51 6817811-7 1982 Measurement of turnover times by incubating the cells with cycloheximide revealed a short turnover time for the enzymic activity tested with exogenous [1-14C]arachidonate (2.3 h) and a relatively long turnover time for the cyclooxygenase activity tested with endogenous substrate released after thrombin treatment of the cells (54 h). Cycloheximide 59-72 coagulation factor II, thrombin Homo sapiens 295-303