PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 3000457-4 1985 Thus, treatment of 3T3-L1 adipocytes with tunicamycin caused the loss of cellular insulin binding activity and the accumulation of an inactive aglyco-proreceptor. Tunicamycin 42-53 insulin Homo sapiens 82-89 3305909-3 1987 Tunicamycin, an inhibitor of N-linked oligosaccharide addition, blocks acquisition of both EGF and insulin binding activity. Tunicamycin 0-11 insulin Homo sapiens 99-106 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. Tunicamycin 134-145 insulin Homo sapiens 14-21 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 83-94 insulin Homo sapiens 42-49 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 83-94 insulin Homo sapiens 118-125 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 83-94 insulin Homo sapiens 118-125 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 150-161 insulin Homo sapiens 42-49 4092492-3 1985 Thus, treatment of 3T3-L1 adipocytes with tunicamycin causes the depletion of cellular insulin binding activity and the accumulation of an inactive aglyco proreceptor. Tunicamycin 42-53 insulin Homo sapiens 87-94 7228853-1 1981 Tunicamycin, which inhibits N-linked oligosaccharide chain addition to nascent polypeptides, interrupts glycosylation of the insulin receptor in 3T3-L1 adipocytes giving rise to inactive receptors. Tunicamycin 0-11 insulin Homo sapiens 125-132 6349621-2 1983 Tunicamycin (1 microgram/ml) induced a steady decrease of insulin binding, which was decreased by 50% after 13 h. As the total number of binding sites per hepatocyte was 20000, the rate of the receptor degradation could not exceed 13 sites/min per hepatocyte. Tunicamycin 0-11 insulin Homo sapiens 58-65 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. Tunicamycin 191-202 insulin Homo sapiens 39-46 7228853-2 1981 Chronic exposure of cells to low levels (100 ng/ml) of high performance liquid chromatography-purified tunicamycin causes a greater than or equal to 90% depletion of insulin binding to cell surface and Triton X-100-extractable receptors and a 93% inhibition of [3H]glucosamine incorporation into protein in alkali-stable form. Tunicamycin 103-114 insulin Homo sapiens 166-173 457783-0 1979 Tunicamycin-mediated depletion of insulin receptors in 3T3-L1 adipocytes. Tunicamycin 0-11 insulin Homo sapiens 34-41 6992777-0 1980 Tunicamycin inhibits the differentiation of ST 13 fibroblasts to adipocytes with suppression of the insulin binding activity. Tunicamycin 0-11 insulin Homo sapiens 100-107 457783-1 1979 Tunicamycin, an antibiotic that inhibits protein glycosylation, elicited a rapid depletion of insulin binding activity at the surface of 3T3-L1 adipocytes. Tunicamycin 0-11 insulin Homo sapiens 94-101 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. Tunicamycin 76-87 insulin Homo sapiens 17-24 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. Tunicamycin 76-87 insulin Homo sapiens 240-247 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. Tunicamycin 76-87 insulin Homo sapiens 240-247 29307512-11 2018 ER stress was readily induced by Tunicamycin and resulted in a reduction of insulin mRNA. Tunicamycin 33-44 insulin Homo sapiens 76-83 32035621-6 2020 Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin. Tunicamycin 160-171 insulin Homo sapiens 0-7 32035621-7 2020 Notably, ATG13 and ULK1 deficiency ameliorated tunicamycin-induced insulin resistance, with enhanced RPS6KB1 and AKT1 phosphorylation in KO cells compared to WT cells. Tunicamycin 47-58 insulin Homo sapiens 67-74 31508171-3 2019 In our study, 3T3-L1 adipocytes were pre-treated with ERS inhibitors tauroursodeoxycholic acid (TUDCA), Ex-4 and an ERS inducer tunicamycin (TM) then induced insulin resistance. Tunicamycin 128-139 insulin Homo sapiens 158-165 31508171-3 2019 In our study, 3T3-L1 adipocytes were pre-treated with ERS inhibitors tauroursodeoxycholic acid (TUDCA), Ex-4 and an ERS inducer tunicamycin (TM) then induced insulin resistance. Tunicamycin 141-143 insulin Homo sapiens 158-165 32660483-4 2020 The purpose of this study is to investigate the effects of CaMKIV on ER stress, autophagic function and insulin signaling in tunicamycin-treated adipocytes. Tunicamycin 125-136 insulin Homo sapiens 104-111 32660483-12 2020 However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes. Tunicamycin 147-158 insulin Homo sapiens 56-63 28246389-6 2017 In in vitro experiments, insulin resistance was induced by applying tunicamycin to HUVECs. Tunicamycin 68-79 insulin Homo sapiens 25-32 28246389-9 2017 Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM. Tunicamycin 110-121 insulin Homo sapiens 46-53 23711134-10 2013 In tunicamycin treatment, HuD and insulin proteins showed similar expression tendencies. Tunicamycin 3-14 insulin Homo sapiens 34-41 24309597-6 2014 Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance. Tunicamycin 0-11 insulin Homo sapiens 80-87 24309597-6 2014 Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance. Tunicamycin 0-11 insulin Homo sapiens 237-244 24309597-7 2014 Moreover, disturbance of autophagy and insulin sensitivity induced by tunicamycin can be effectively corrected by the addition of osteocalcin in an NFkappaB-dependent manner in vitro. Tunicamycin 70-81 insulin Homo sapiens 39-46 24652289-7 2014 Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1). Tunicamycin 57-68 insulin Homo sapiens 122-129 22374970-6 2012 Strikingly, exposure of HepG2 cells to prolonged mild ER stress activation induced by low levels of thapsigargin, tunicamycin, or palmitate augmented insulin-stimulated Akt phosphorylation. Tunicamycin 114-125 insulin Homo sapiens 150-157 2269328-3 1990 Furthermore, presentation of the insulin fragment as well as presentation of ovalbumin (OVA) was inhibited by treatment of APC with chloroquine, cerulenin or tunicamycin. Tunicamycin 158-169 insulin Homo sapiens 33-40 21076579-5 2010 METHODS: The effects of tunicamycin and thapsigargin on insulin and TRB3 expression in INS-1 cells were measured by Northern and Western blot analysis, respectively. Tunicamycin 24-35 insulin Homo sapiens 56-63 22281494-2 2012 Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes. Tunicamycin 29-40 insulin Homo sapiens 80-87 22006247-6 2012 RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt). Tunicamycin 50-61 insulin Homo sapiens 72-79