PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27344174-7	2016	Pharmacological inhibition of LAT1 increased the growth inhibitory effects and the inactivation of the mTOR pathway resulting from glycosylation defects, an effect further emphasized during the regrowth period post-treatment with tunicamycin.	Tunicamycin	230-241	mechanistic target of rapamycin kinase	Homo sapiens	103-107	
29130967-6	2017	The mutant p53 cell lines were treated with tunicamycin to induce ERS and rapamycin in order to inhibit mTOR.	Tunicamycin	44-55	mechanistic target of rapamycin kinase	Homo sapiens	104-108	
20685651-3	2010	We found that overexpression of lipid-anchored Rheb enhanced the apoptotic effects induced by UV light, TNFalpha, or tunicamycin in an mTOR complex 1 (mTORC1)-dependent manner.	Tunicamycin	117-128	mechanistic target of rapamycin kinase	Homo sapiens	135-139	
25428129-6	2015	Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K.	Tunicamycin	49-60	mechanistic target of rapamycin kinase	Homo sapiens	15-19	
25428129-6	2015	Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K.	Tunicamycin	49-60	mechanistic target of rapamycin kinase	Homo sapiens	112-116	
25428129-7	2015	Inhibition of mTOR with rapamycin partially suppressed the phosphorylation of PERK and eIF2a and the induction of CHOP and GRP78 induction during tunicamycin treatment.	Tunicamycin	146-157	mechanistic target of rapamycin kinase	Homo sapiens	14-18	
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	mechanistic target of rapamycin kinase	Homo sapiens	178-182	
30657961-6	2019	We found that ER stress marker GRP78 expression increased with CHOP and TRIB3 expression in normal endometrial stromal cells (NESCs) treated with tunicamycin, and this increase was accompanied by decreased AKT and mTOR activity and cellular invasiveness.	Tunicamycin	146-157	mechanistic target of rapamycin kinase	Homo sapiens	214-218	
20104019-3	2010	Three widely used ER stress inducers including tunicamycin, DTT and MG132 led to the conversion of LC3-I to LC3-II , a commonly used marker of autophagy, as well as the downregulation of mTOR concurrently.	Tunicamycin	47-58	mechanistic target of rapamycin kinase	Homo sapiens	187-191	
32660483-6	2020	Tunicamycin-treated 3 T3-L1 adipocytes were treated with recombinant CaMKIV in the presence or absence of targeted-siRNA mediated down-regulation of CREB and mTOR.	Tunicamycin	0-11	mechanistic target of rapamycin kinase	Homo sapiens	158-162	
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	mechanistic target of rapamycin kinase	Homo sapiens	131-135	
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	mechanistic target of rapamycin kinase	Homo sapiens	239-243	
29344654-0	2018	Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway.	Tunicamycin	0-11	mechanistic target of rapamycin kinase	Homo sapiens	106-110	
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	mechanistic target of rapamycin kinase	Homo sapiens	217-246	
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	mechanistic target of rapamycin kinase	Homo sapiens	248-252	
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	mechanistic target of rapamycin kinase	Homo sapiens	95-99	
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	mechanistic target of rapamycin kinase	Homo sapiens	95-99	
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	mechanistic target of rapamycin kinase	Homo sapiens	139-143	
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	mechanistic target of rapamycin kinase	Homo sapiens	139-143	
29154199-6	2018	Importantly, UVB treatment perturbs the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and LC3-II turnover in response to treatment with MTOR inhibitors (Torin 1 and pp242), as well as endoplasmic reticular stress (A23187 and tunicamycin), inositol pathway (L690,330) and autophagy inducers (resveratrol and STF62247).	Tunicamycin	258-269	mechanistic target of rapamycin kinase	Homo sapiens	169-173	
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	mechanistic target of rapamycin kinase	Homo sapiens	178-182	
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	mechanistic target of rapamycin kinase	Homo sapiens	220-224	
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	mechanistic target of rapamycin kinase	Homo sapiens	150-154	
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	mechanistic target of rapamycin kinase	Homo sapiens	157-161	
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	mechanistic target of rapamycin kinase	Homo sapiens	214-218