PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25792980-5 2015 To determine whether insulin affects SESN2 degradation, we assessed SESN2 turnover by applying the protein synthesis inhibitor, cycloheximide (CHX), and found that following insulin treatment SESN2 protein levels were reduced significantly slower than non-insulin-treated cells. Cycloheximide 128-141 insulin Homo sapiens 174-181 25792980-5 2015 To determine whether insulin affects SESN2 degradation, we assessed SESN2 turnover by applying the protein synthesis inhibitor, cycloheximide (CHX), and found that following insulin treatment SESN2 protein levels were reduced significantly slower than non-insulin-treated cells. Cycloheximide 128-141 insulin Homo sapiens 174-181 24405299-5 2014 Interestingly, treatment with the protein synthesis inhibitor cycloheximide and the ER-Golgi trafficking blocker Brefeldin A inhibit both basal and ISLS (insulin-stimulated leptin secretion), suggesting that insulin stimulates leptin secretion by up-regulating leptin synthesis and that leptin-containing vesicles go through the ER-Golgi route. Cycloheximide 62-75 insulin Homo sapiens 154-161 24405299-5 2014 Interestingly, treatment with the protein synthesis inhibitor cycloheximide and the ER-Golgi trafficking blocker Brefeldin A inhibit both basal and ISLS (insulin-stimulated leptin secretion), suggesting that insulin stimulates leptin secretion by up-regulating leptin synthesis and that leptin-containing vesicles go through the ER-Golgi route. Cycloheximide 62-75 insulin Homo sapiens 208-215 15326561-4 2004 Although the increase by insulin in these cells was inhibited by treatment with actinomycin D, this was enhanced by treatment with cycloheximide. Cycloheximide 131-144 insulin Homo sapiens 25-32 21513489-6 2011 The insulin-induced resistance to cycloheximide and 5-fluorouracil can be used in drug screening to overcome the inefficacy of chemotherapy in obesity-associated colon cancer. Cycloheximide 34-47 insulin Homo sapiens 4-11 16506055-6 2006 The insulin-induced increase of HIF-1alpha is blunted by the translation inhibitor cycloheximide, LY294002, PD98059, SP600125 and rapamycin, but not by SB203580. Cycloheximide 83-96 insulin Homo sapiens 4-11 14749039-7 2004 Semi-quantitative RT-PCR and Southern blotting showed that insulin also increased P-LAP mRNA, which was abrogated by prior exposure to cycloheximide. Cycloheximide 135-148 insulin Homo sapiens 59-66 11779863-2 2002 Similar to TNF, cycloheximide and anisomycin stimulated serine phosphorylation of IRS-1 and IRS-2, reduced their ability to interact with the insulin receptor, inhibited the insulin-induced tyrosine phosphorylation of IRS proteins, and diminished their association with phosphatidylinositol 3-kinase (PI3K). Cycloheximide 16-29 insulin Homo sapiens 142-149 12627322-8 2003 Cycloheximide, a protein synthesis inhibitor, completely blocked insulin-induced reduction of resistin mRNA. Cycloheximide 0-13 insulin Homo sapiens 65-72 12007784-6 2002 Furthermore, insulin induced ubiquitous PFK-2 protein levels, that were evident after a lag of 3 h and could be inhibited by incubation with cycloheximide. Cycloheximide 141-154 insulin Homo sapiens 13-20 11549696-5 2001 A maximal stimulation of the basal level up to 192% was found with 10 nmol/liter insulin after 24 h. Actinomycin D and cycloheximide abolished this effect, providing evidence that active RNA and protein synthesis are involved in insulin"s action. Cycloheximide 119-132 insulin Homo sapiens 81-88 11696451-7 2001 Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. Cycloheximide 140-153 insulin Homo sapiens 0-7 11696451-7 2001 Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. Cycloheximide 140-153 insulin Homo sapiens 112-119 9844728-2 1998 We found that AA acted synergistically with cycloheximide to suppress insulin-stimulated glucose transport, although it alone was without effect. Cycloheximide 44-57 insulin Homo sapiens 70-77 9844728-4 1998 Immunoblot analysis indicated that the increase in plasma membranes of the insulin-regulated glucose transporter (GLUT4) in response to insulin was decreased in cells pretreated with cycloheximide for a prolonged time, while total amount of GLUT4 was not altered. Cycloheximide 183-196 insulin Homo sapiens 75-82 9844728-4 1998 Immunoblot analysis indicated that the increase in plasma membranes of the insulin-regulated glucose transporter (GLUT4) in response to insulin was decreased in cells pretreated with cycloheximide for a prolonged time, while total amount of GLUT4 was not altered. Cycloheximide 183-196 insulin Homo sapiens 136-143 7532054-5 1994 The stimulation of IGFBP-2 by IGF-I and insulin was reversibly abolished by incubation with protein synthesis inhibitors such as cycloheximide. Cycloheximide 129-142 insulin Homo sapiens 40-47 9618150-2 1998 At physiological doses, either insulin-like growth factor I (IGF-I) or insulin turned out to be as potent as dibutyryl cAMP (dbcAMP) in increasing UCP1 gene transcription rate (1 h) and also UCP1 mRNA accumulation (3 h), their maximal effect (15-fold increase) reached upon treatment for 24 h. Upon treatment with either IGF-I or insulin for 48 h, a 7-fold increase in the UCP1 protein content relative to levels in the control cells was found, this induction being abolished in the presence of cycloheximide. Cycloheximide 495-508 insulin Homo sapiens 31-38 7667244-7 1995 Substances that block glucose transport (100 microM cytochalasin B) and protein synthesis (1 mM cycloheximide) also markedly reduced insulin biosynthesis. Cycloheximide 96-109 insulin Homo sapiens 133-140 7883838-6 1995 The insulin-induced ET-1 secretion was inhibited by genistein, a tyrosine kinase inhibitor, and by cycloheximide, a protein synthesis inhibitor, suggesting that it requires de novo protein synthesis rather than ET-1 release from intracellular stores. Cycloheximide 99-112 insulin Homo sapiens 4-11 9618150-2 1998 At physiological doses, either insulin-like growth factor I (IGF-I) or insulin turned out to be as potent as dibutyryl cAMP (dbcAMP) in increasing UCP1 gene transcription rate (1 h) and also UCP1 mRNA accumulation (3 h), their maximal effect (15-fold increase) reached upon treatment for 24 h. Upon treatment with either IGF-I or insulin for 48 h, a 7-fold increase in the UCP1 protein content relative to levels in the control cells was found, this induction being abolished in the presence of cycloheximide. Cycloheximide 495-508 insulin Homo sapiens 71-78 9094251-10 1997 This finding suggests that the cycloheximide-sensitive step of the action of insulin is related to Na+ delivery to the pump. Cycloheximide 31-44 insulin Homo sapiens 77-84 8835848-10 1996 The insulin-induced increase in pro-alpha 1 (I) collagen mRNA was blocked by the presence of cycloheximide indicating a requirement for new protein synthesis. Cycloheximide 93-106 insulin Homo sapiens 4-11 1384465-6 1992 The formation of cGMP does not appear to mediate the inhibitory effects of IL-1 beta on insulin secretion since a concentration of cycloheximide (1 microM) that blocks IL-1 beta-induced inhibition of glucose-stimulated insulin secretion and nitric oxide formation does not prevent cGMP accumulation, thus dissociating the two events. Cycloheximide 131-144 insulin Homo sapiens 219-226 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 insulin Homo sapiens 61-68 1483963-2 1992 In the present study we investigated the effect of insulinlike growth factor-1, insulin, and epidermal growth factor on cell death induced by cycloheximide in the confluent MCF-7 cells, and correlated this effect to the inhibition rate of protein synthesis. Cycloheximide 142-155 insulin Homo sapiens 51-58 1634442-0 1992 Serum and insulin inhibit cell death induced by cycloheximide in the human breast cancer cell line MCF-7. Cycloheximide 48-61 insulin Homo sapiens 10-17 1618850-5 1992 In both transfectants, the maximal insulin-induced increase (approximately 3.5-fold) in uptake was cycloheximide-sensitive and was paralleled by equivalent increases in the levels of GLUT-1 immunoreactive protein and mRNA. Cycloheximide 99-112 insulin Homo sapiens 35-42 1874723-4 1991 The insulin-induced loss of the intact beta subunit from the cellular membranes is inhibited by cycloheximide. Cycloheximide 96-109 insulin Homo sapiens 4-11 1719559-6 1991 A 10- to 20-fold increase in IGF binding protein I mRNA was seen 16-48 hr after exposure of the HepG2 cells to insulin and IGF-I, an increase abolished by cycloheximide. Cycloheximide 155-168 insulin Homo sapiens 111-118 1601743-7 1992 Cycloheximide, but no actinomycin D, inhibited the effect of insulin on androgen receptor binding. Cycloheximide 0-13 insulin Homo sapiens 61-68 2037570-3 1991 Exposure of these cells to 300 microM anisomycin or 500 microM cycloheximide caused a maximal, 7-fold increase in 2-deoxyglucose transport rate after 4-8 h. The effects due to either insulin (0.5 h) or anisomycin (5 h) on the kinetics of zero-trans 3-O-methyl[14C]glucose transport were similar, resulting in 2.5-3-fold increases in apparent Vmax values (control Vmax = 1.6 +/- 0.3 x 10(-7) mmol/s/10(6) cells) coupled with approximately 2-fold decreases in apparent Km values (control Km = 23 +/- 3.3 mM). Cycloheximide 63-76 insulin Homo sapiens 183-190 1677644-11 1991 The use of cycloheximide indicated that the effect of insulin on alpha 2-adrenergic receptor mRNA does not require protein synthesis. Cycloheximide 11-24 insulin Homo sapiens 54-61 1910304-3 1991 The time course of glycogen synthase activation measured by the activity ratio (low G-6-P/high G-6-P) in response to insulin was biphasic with the first peak at 15 min and the second peak at 4 to 6 h. When cells were incubated with insulin and cycloheximide, the first peak persisted while the second peak was abolished. Cycloheximide 244-257 insulin Homo sapiens 117-124 1999176-8 1991 The insulin-induced stimulation of hCG synthesis was inhibited by cycloheximide. Cycloheximide 66-79 insulin Homo sapiens 4-11 1989989-4 1991 Pretreatment of cells with cycloheximide completely inhibited insulin-stimulated ODC expression; actinomycin D partially inhibited this effect. Cycloheximide 27-40 insulin Homo sapiens 62-69 2168170-6 1990 Cycloheximide partially blocked the induction of GLUT1 mRNA by insulin but not by glucose deprivation. Cycloheximide 0-13 insulin Homo sapiens 63-70 2229049-2 1990 Moreover, it appears that glucose modulates insulin receptor affinity through de novo protein synthesis rather than through covalent modification of receptors, since cycloheximide selectively inhibited the glucose-induced increase in insulin binding capacity (ED50 of 360 ng/ml) and restored receptor affinity to control values. Cycloheximide 166-179 insulin Homo sapiens 44-51 2163613-8 1990 The most striking effects of PMA and insulin on Fru-2,6-P2 production are observed after long-term treatment (24 h) and are abolished by actinomycin, cycloheximide and puromycin, suggesting that protein synthesis is involved. Cycloheximide 150-163 insulin Homo sapiens 37-44 3041200-3 1987 Cycloheximide blocked the action of insulin on glycogen synthase, glycogen synthase phosphatase and phosphorylase phosphatase. Cycloheximide 0-13 insulin Homo sapiens 36-43 2156894-5 1990 Simultaneous addition of 2 microM cycloheximide prevented the insulin-induced decline in resistance; in fact, this combination caused a significant increase in electrical resistance. Cycloheximide 34-47 insulin Homo sapiens 62-69 2196901-4 1990 Actinomycin D and cycloheximide inhibited the insulin-stimulated expression of chromatin receptors. Cycloheximide 18-31 insulin Homo sapiens 46-53 2537240-7 1989 An accumulation of receptors at the cell surface was observed in the absence of de novo protein synthesis, since cycloheximide caused a significant increase in insulin binding to the cells. Cycloheximide 113-126 insulin Homo sapiens 160-167 2551637-6 1989 Insulin- and IGF-I-stimulated 3 beta HSD activities were completely inhibited by concurrent treatment with either actinomycin-D or cycloheximide, suggesting that new mRNA and protein synthesis are required for these peptides to exert their effects. Cycloheximide 131-144 insulin Homo sapiens 0-7 2838341-0 1988 [Modification by cycloheximide of the effects of insulin on the transport of calcium by sarcolemma of the myocardium]. Cycloheximide 17-30 insulin Homo sapiens 49-56 2838341-3 1988 Pretreatment of myocardial preparation with cycloheximide in low concentrations completely blocks the inhibitory insulin effect on Ca2+-current due, probably, to a decrease in peptide formation. Cycloheximide 44-57 insulin Homo sapiens 113-120 2838341-5 1988 Possible mechanisms of modifying effect of cycloheximide on the function of insulin-dependent regulatory system in the myocardium, are discussed. Cycloheximide 43-56 insulin Homo sapiens 76-83 3539932-1 1987 Cycloheximide, a potent inhibitor of protein synthesis, has been used to examine the relationship between recruitment of hexose carriers and the activation of glucose transport by insulin in rat adipocytes. Cycloheximide 0-13 insulin Homo sapiens 180-187 3539932-8 1987 When isolated membranes were analyzed with an antiserum prepared against human erythrocyte glucose transporter, decreased cross-reactivity was observed in plasma membranes prepared from cycloheximide/insulin-treated cells compared to those from insulin cells. Cycloheximide 186-199 insulin Homo sapiens 200-207 3539932-9 1987 The present findings indicate that incubation of adipocytes with cycloheximide greatly reduces the number of hexose carriers in the plasma membrane of insulin-stimulated cells. Cycloheximide 65-78 insulin Homo sapiens 151-158 3902825-6 1985 In the presence of extracellular insulin, this effect of cycloheximide resulted in the long-term (6 h) accumulation of receptor in a trypsin-resistant intracellular compartment. Cycloheximide 57-70 insulin Homo sapiens 33-40 3535799-7 1986 Cycloheximide which blocked the glucose refeeding effect on hexose transport, decreased the ability of insulin to stimulate hexose transport. Cycloheximide 0-13 insulin Homo sapiens 103-110 3535799-8 1986 Specific 125I-insulin binding was increased by glucose refeeding of glucose-starved cells and this change in binding was inhibited by tunicamycin and cycloheximide. Cycloheximide 150-163 insulin Homo sapiens 14-21 2999163-10 1985 Cycloheximide did not prevent the increased basal glucose incorporation in glucose-starved cells, but markedly inhibited the insulin response, while in glucose-fed cells, cycloheximide stimulated basal glucose incorporation. Cycloheximide 0-13 insulin Homo sapiens 125-132 3882760-4 1985 The insulin resistance activity was decreased by coincubation with the protein synthesis inhibitor, cycloheximide. Cycloheximide 100-113 insulin Homo sapiens 4-11 3928421-4 1985 However, insulin-induced downregulation of insulin receptors was: (1) demonstrable in receptor-positive cells, (2) dependent on insulin concentration, (3) temporally unrelated to insulin internalization, and (4) prevented by culture at 4 degrees C but not by cycloheximide at 37 degrees C. Recovery of insulin receptors required further culture of cells in media depleted of insulin for 24 h. Scatchard analysis revealed loss of receptor number without changes in receptor affinity. Cycloheximide 259-272 insulin Homo sapiens 9-16 3928421-4 1985 However, insulin-induced downregulation of insulin receptors was: (1) demonstrable in receptor-positive cells, (2) dependent on insulin concentration, (3) temporally unrelated to insulin internalization, and (4) prevented by culture at 4 degrees C but not by cycloheximide at 37 degrees C. Recovery of insulin receptors required further culture of cells in media depleted of insulin for 24 h. Scatchard analysis revealed loss of receptor number without changes in receptor affinity. Cycloheximide 259-272 insulin Homo sapiens 43-50 3928421-4 1985 However, insulin-induced downregulation of insulin receptors was: (1) demonstrable in receptor-positive cells, (2) dependent on insulin concentration, (3) temporally unrelated to insulin internalization, and (4) prevented by culture at 4 degrees C but not by cycloheximide at 37 degrees C. Recovery of insulin receptors required further culture of cells in media depleted of insulin for 24 h. Scatchard analysis revealed loss of receptor number without changes in receptor affinity. Cycloheximide 259-272 insulin Homo sapiens 43-50 3928421-4 1985 However, insulin-induced downregulation of insulin receptors was: (1) demonstrable in receptor-positive cells, (2) dependent on insulin concentration, (3) temporally unrelated to insulin internalization, and (4) prevented by culture at 4 degrees C but not by cycloheximide at 37 degrees C. Recovery of insulin receptors required further culture of cells in media depleted of insulin for 24 h. Scatchard analysis revealed loss of receptor number without changes in receptor affinity. Cycloheximide 259-272 insulin Homo sapiens 43-50 3928421-4 1985 However, insulin-induced downregulation of insulin receptors was: (1) demonstrable in receptor-positive cells, (2) dependent on insulin concentration, (3) temporally unrelated to insulin internalization, and (4) prevented by culture at 4 degrees C but not by cycloheximide at 37 degrees C. Recovery of insulin receptors required further culture of cells in media depleted of insulin for 24 h. Scatchard analysis revealed loss of receptor number without changes in receptor affinity. Cycloheximide 259-272 insulin Homo sapiens 43-50 3928421-4 1985 However, insulin-induced downregulation of insulin receptors was: (1) demonstrable in receptor-positive cells, (2) dependent on insulin concentration, (3) temporally unrelated to insulin internalization, and (4) prevented by culture at 4 degrees C but not by cycloheximide at 37 degrees C. Recovery of insulin receptors required further culture of cells in media depleted of insulin for 24 h. Scatchard analysis revealed loss of receptor number without changes in receptor affinity. Cycloheximide 259-272 insulin Homo sapiens 43-50 6376245-5 1984 Cycloheximide (20 micrograms/ml), a translational inhibitor of protein synthesis, prevented the insulin-mediated increase in the enzyme activity and the incorporation of 14C-acetate into sterols. Cycloheximide 0-13 insulin Homo sapiens 96-103 6373768-6 1984 Cycloheximide (and puromycin) pretreatment prevented insulin-induced increases in phospholipids and rapidly reversed ongoing insulin effects on phospholipids and pyruvate dehydrogenase activity. Cycloheximide 0-13 insulin Homo sapiens 53-60 6373768-6 1984 Cycloheximide (and puromycin) pretreatment prevented insulin-induced increases in phospholipids and rapidly reversed ongoing insulin effects on phospholipids and pyruvate dehydrogenase activity. Cycloheximide 0-13 insulin Homo sapiens 125-132 6410926-6 1983 Coincident with this effect, insulin increased the lipoprotein lipase activity fraction inhibitable by cycloheximide (0.01 mg/ml), and the immunotitratable enzyme activity. Cycloheximide 103-116 insulin Homo sapiens 29-36 6349621-3 1983 Cycloheximide (2.8 micrograms/ml) increased insulin binding by 30% within 6 h, an effect that persisted for up to 25 h. This drug had a specific inhibitory effect on the degradation of proteins prelabelled for 10 h with [14C]glucosamine, without affecting the degradation of total proteins. Cycloheximide 0-13 insulin Homo sapiens 44-51 6349621-7 1983 First, the rate of release of degraded insulin into the medium was 600 molecules/min per hepatocyte with 1 nM labelled hormone, and increased (preincubation with cycloheximide) or decreased (tunicamycin) as a function of the amount of cell-bound insulin. Cycloheximide 162-175 insulin Homo sapiens 39-46 4526203-6 1974 The effects of insulin were prevented by cycloheximide and are probably due to an increased synthesis of 3-hydroxy-3-methylglutaryl CoA reductase or of a protein that regulates its activity. Cycloheximide 41-54 insulin Homo sapiens 15-22 7031662-9 1981 The acceleration of receptor degradation induced by insulin was partially blocked by 100 microM cycloheximide. Cycloheximide 96-109 insulin Homo sapiens 52-59 6792927-5 1981 Serine-induced increases in insulin binding were detectable after 15 min of incubation and were abolished by the addition of cycloheximide (1 micrograms/ml) but not by actinomycin D (1 microgram/ml). Cycloheximide 125-138 insulin Homo sapiens 28-35 7024288-6 1981 Protein synthesis furthermore does not seem to be required, since a significant insulin effect can be seen in the presence of the protein synthesis inhibitor, cycloheximide. Cycloheximide 159-172 insulin Homo sapiens 80-87 185104-5 1975 Only cycloheximide was found to significantly reduce the synthesis and subsequent release of insulin-like peptides by the tumoral tissue. Cycloheximide 5-18 insulin Homo sapiens 93-100 7048676-2 1982 Extracts from the embryos preliminary affected by insulin possessed a lower stabilizing ability, the hormonal effect being removed to a considerable extent by actinomycin D and cycloheximide. Cycloheximide 177-190 insulin Homo sapiens 50-57 6749717-2 1982 The amount of 125I-insulin bound to the cell surface was found to remain relatively constant during times of active insulin degradation over a wide range of insulin concentrations, even in the presence of cycloheximide. Cycloheximide 205-218 insulin Homo sapiens 19-26 457783-2 1979 Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anti-insulin receptor antibody on hexose uptake and metabolism. Cycloheximide 133-146 insulin Homo sapiens 17-24 196374-1 1977 It is established that in embryos incubated until the early blastula stage in the solution of insulin with addition of cycloheximide or puromycin, there is neither a decrease in the hexokinase and glucose-61 phosphate dehydrogenase activities nor an increase in the phosphofructokinase activity, as it is shown under the influence of insulin only. Cycloheximide 119-132 insulin Homo sapiens 94-101 5093122-0 1971 The effect of cycloheximide and 2-deoxyglucose on the diphasic pattern of insulin secretion. Cycloheximide 14-27 insulin Homo sapiens 74-81 4291105-3 1967 The transfer of about 70 percent of the radioactivity of the larger protein to insulin was demonstrated in the absence of new peptide bond synthesis (cycloheximide), or during incubation with unlabeled amino acid (chase). Cycloheximide 150-163 insulin Homo sapiens 79-86