PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29344654-0 2018 Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway. Tunicamycin 0-11 AKT serine/threonine kinase 1 Homo sapiens 102-105 31888113-6 2019 Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells. Tunicamycin 44-55 AKT serine/threonine kinase 1 Homo sapiens 207-210 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 182-193 AKT serine/threonine kinase 1 Homo sapiens 135-138 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 AKT serine/threonine kinase 1 Homo sapiens 98-127 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 AKT serine/threonine kinase 1 Homo sapiens 129-133 30483742-0 2019 Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-kappaB signaling pathway. Tunicamycin 0-11 AKT serine/threonine kinase 1 Homo sapiens 111-114 29344654-8 2018 Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells. Tunicamycin 39-50 AKT serine/threonine kinase 1 Homo sapiens 197-200 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 43-54 AKT serine/threonine kinase 1 Homo sapiens 87-90 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 134-145 AKT serine/threonine kinase 1 Homo sapiens 87-90 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 44-55 AKT serine/threonine kinase 1 Homo sapiens 135-138 28537902-3 2017 Increasing concentrations of tunicamycin and CDDP activated ERS in SKOV3 cells, reduced cell viability and proliferation, increased apoptosis and autophagy, enhanced expression of ERS-related proteins, and inhibited expression of PI3K/AKT/mTOR pathway-related proteins. Tunicamycin 29-40 AKT serine/threonine kinase 1 Homo sapiens 235-238 28453460-1 2017 OBJECTIVE: The study is to explore the role of tunicamycin-induced endoplasmic reticulum stress (ERS) in human ovarian cancer (OC) SKOV3 cells proliferation, migration and invasion by modulating the activity of PI3K/AKT/mTOR pathway. Tunicamycin 47-58 AKT serine/threonine kinase 1 Homo sapiens 216-219 28453460-11 2017 CONCLUSION: The study provides strong evidence that tunicamycin-induced ERS induces the apoptosis of human OC SKOV3 cells through inhibiting PI3K/AKT/mTOR signaling pathway. Tunicamycin 52-63 AKT serine/threonine kinase 1 Homo sapiens 146-149 23658755-9 2013 However, co-pretreatment with tunicamycin and Pae decreased the expression of COX-2 and levels of activation of Akt as well as increasing the levels of CHOP in HCC cells. Tunicamycin 30-41 AKT serine/threonine kinase 1 Homo sapiens 112-115 28978049-5 2017 We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment. Tunicamycin 54-65 AKT serine/threonine kinase 1 Homo sapiens 104-107 28631572-10 2017 With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins. Tunicamycin 19-30 AKT serine/threonine kinase 1 Homo sapiens 174-177 28459209-10 2017 In MCF-7 cells treated with tunicamycin, cell viability decreased significantly, but PEAK, eIF2, and CHOP were upregulated markedly and p-PI3K, p-AKT, and p-MTOR were downregulated in dose- and time-dependent manners. Tunicamycin 28-39 AKT serine/threonine kinase 1 Homo sapiens 146-149 28459209-14 2017 Our study provide evidence that endoplasmic reticulum stress activated by tunicamycin could promote breast cancer cell autophagy and apoptosis and enhance chemosensitivity of MCF-7 cells by inhibiting the PI3K/AKT/mTOR signaling pathway. Tunicamycin 74-85 AKT serine/threonine kinase 1 Homo sapiens 210-213 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 AKT serine/threonine kinase 1 Homo sapiens 83-86 27603596-6 2017 In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin. Tunicamycin 13-24 AKT serine/threonine kinase 1 Homo sapiens 121-124 27603596-6 2017 In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin. Tunicamycin 236-247 AKT serine/threonine kinase 1 Homo sapiens 121-124 23711089-8 2013 Simultaneously, the expression of phosphorylated AKT (p-AKT) was elevated in HepG2 and SMMC-7721 cells given tunicamycin but reduced in the presence of melatonin. Tunicamycin 109-120 AKT serine/threonine kinase 1 Homo sapiens 49-52 23711089-8 2013 Simultaneously, the expression of phosphorylated AKT (p-AKT) was elevated in HepG2 and SMMC-7721 cells given tunicamycin but reduced in the presence of melatonin. Tunicamycin 109-120 AKT serine/threonine kinase 1 Homo sapiens 56-59 19424594-5 2009 Importantly, both PI3K inhibitor LY294002 and dominant-negative Akt construct promoted tunicamycin- and thapsigargin-induced ERK phosphorylation. Tunicamycin 87-98 AKT serine/threonine kinase 1 Homo sapiens 64-67 17167073-8 2007 Transient overexpression of wild-type Akt, but not kinase-dead Akt, in JEG-3 cells diminished tunicamycin-OGD reoxygenation-induced apoptosis. Tunicamycin 94-105 AKT serine/threonine kinase 1 Homo sapiens 38-41 16375864-4 2006 Treatment with tunicamycin or thapsigargin, ER stress inducers, caused dephosphorylation of Akt from 12 to 24 h and induced cell death. Tunicamycin 15-26 AKT serine/threonine kinase 1 Homo sapiens 92-95 20020442-5 2010 Interestingly, in thapsigargin and tunicamycin-stressed chondrocytes induction of the proapoptotic transcription factor CHOP preceded that of the anti-apoptotic BiP by 12 h. Although both of these agents caused sustained Akt and ERK phosphorylation; inhibition of Akt phosphorylation sensitized chondrocytes to ER stress, while blocking ERK signaling by U0126 had no effect. Tunicamycin 35-46 AKT serine/threonine kinase 1 Homo sapiens 221-224 20020442-5 2010 Interestingly, in thapsigargin and tunicamycin-stressed chondrocytes induction of the proapoptotic transcription factor CHOP preceded that of the anti-apoptotic BiP by 12 h. Although both of these agents caused sustained Akt and ERK phosphorylation; inhibition of Akt phosphorylation sensitized chondrocytes to ER stress, while blocking ERK signaling by U0126 had no effect. Tunicamycin 35-46 AKT serine/threonine kinase 1 Homo sapiens 264-267 15339911-3 2004 Here, we have shown that endogenous Akt and ERK are rapidly activated and act as downstream effectors of phosphatidylinositol 3-kinase in thapsigargin- or tunicamycin-induced ER stress. Tunicamycin 155-166 AKT serine/threonine kinase 1 Homo sapiens 36-39