PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 mitogen-activated protein kinase 8 Homo sapiens 122-125 29344654-0 2018 Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway. Tunicamycin 0-11 mitogen-activated protein kinase 8 Homo sapiens 89-92 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 mitogen-activated protein kinase 8 Homo sapiens 145-174 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 mitogen-activated protein kinase 8 Homo sapiens 82-85 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 mitogen-activated protein kinase 8 Homo sapiens 82-85 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 mitogen-activated protein kinase 8 Homo sapiens 122-125 28024901-7 2017 On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation. Tunicamycin 58-69 mitogen-activated protein kinase 8 Homo sapiens 121-124 27915415-0 2017 Exendin-4 protects HUVECs from tunicamycin-induced apoptosis via inhibiting the IRE1a/JNK/caspase-3 pathway. Tunicamycin 31-42 mitogen-activated protein kinase 8 Homo sapiens 86-89 27915415-8 2017 Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4. Tunicamycin 109-120 mitogen-activated protein kinase 8 Homo sapiens 49-52 27915415-8 2017 Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4. Tunicamycin 109-120 mitogen-activated protein kinase 8 Homo sapiens 53-56 27603596-0 2017 Tunicamycin enhances human colon cancer cells to TRAIL-induced apoptosis by JNK-CHOP-mediated DR5 upregulation and the inhibition of the EGFR pathway. Tunicamycin 0-11 mitogen-activated protein kinase 8 Homo sapiens 76-79 27603596-7 2017 In summary, tunicamycin effectively enhanced TRAIL-induced apoptosis might through JNK-CHOP-mediated DR5 upregulation and the inhibition of the epidermal growth factor receptor pathway. Tunicamycin 12-23 mitogen-activated protein kinase 8 Homo sapiens 83-86 22006247-10 2012 Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation. Tunicamycin 8-19 mitogen-activated protein kinase 8 Homo sapiens 118-121 24784707-8 2014 This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. Tunicamycin 68-79 mitogen-activated protein kinase 8 Homo sapiens 88-111 24784707-8 2014 This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. Tunicamycin 68-79 mitogen-activated protein kinase 8 Homo sapiens 113-116 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 mitogen-activated protein kinase 8 Homo sapiens 160-163 26851027-3 2016 Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene. Tunicamycin 109-120 mitogen-activated protein kinase 8 Homo sapiens 403-426 26851027-3 2016 Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene. Tunicamycin 109-120 mitogen-activated protein kinase 8 Homo sapiens 428-431 17283057-4 2007 The requirement of the p85alpha regulatory subunit for JNK occurs independently of its role as a component of the PI3K heterodimer and occurs only in response to specific stimuli, namely, insulin and tunicamycin, a chemical that induces endoplasmic reticulum stress. Tunicamycin 200-211 mitogen-activated protein kinase 8 Homo sapiens 55-58 18544642-8 2008 In vitro, palmitate, thapsigargin, and tunicamycin but not oleate induced endoplasmic reticulum stress in HepG2 cells, including increased transcripts CHOP, ERN1, GADD34, and PERK, and increased XBP1 splicing along with phosphorylation of eukaryotic initiation factor eIF2alpha, JNK1, and c-jun. Tunicamycin 39-50 mitogen-activated protein kinase 8 Homo sapiens 279-283 16357177-4 2005 Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism. Tunicamycin 90-101 mitogen-activated protein kinase 8 Homo sapiens 126-153 16357177-4 2005 Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism. Tunicamycin 90-101 mitogen-activated protein kinase 8 Homo sapiens 155-158 34533242-7 2021 Biochemical experiments further discovered that rosamultin could inhibit p38 and JNK activation, and downregulate the levels of CHOP and proteins in its upstream PERK-eIF2alpha-ATF4 signaling pathway stimulated by cisplatin or tunicamycin. Tunicamycin 227-238 mitogen-activated protein kinase 8 Homo sapiens 81-84 16166642-3 2005 Elevated expression of JAMP following UV or tunicamycin treatment results in sustained JNK activity and a higher level of JNK-dependent apoptosis. Tunicamycin 44-55 mitogen-activated protein kinase 8 Homo sapiens 87-90 16166642-3 2005 Elevated expression of JAMP following UV or tunicamycin treatment results in sustained JNK activity and a higher level of JNK-dependent apoptosis. Tunicamycin 44-55 mitogen-activated protein kinase 8 Homo sapiens 122-125