PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30429217-6	2019	Interestingly, calreticulin was sufficient for attenuating ER stress in tunicamycin- or thapsigargin-treated HeLa cells, whereas lentivirus-mediated shRNA calreticulin knockdown exacerbated ER stress.	Tunicamycin	72-83	calreticulin	Homo sapiens	15-27	
33209200-7	2020	The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells.	Tunicamycin	138-140	calreticulin	Homo sapiens	35-39	
33209200-7	2020	The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells.	Tunicamycin	138-140	calreticulin	Homo sapiens	64-68	
35514983-4	2022	We found that microglia release nanomolar levels of calreticulin when inflammatory-activated with lipopolysaccharide, when endoplasmic reticulum stress was induced by tunicamycin, or when cell death was induced by staurosporine, and that neurons release calreticulin when crushed.	Tunicamycin	167-178	calreticulin	Homo sapiens	52-64	
24807724-5	2014	CRT was also found to be of high importance for proper oligomerization of the viral structural proteins VP26 and VP28, and when CRT glycosylation was blocked with tunicamycin, a significant decrease in both viral replication and assembly was detected.	Tunicamycin	163-174	calreticulin	Homo sapiens	0-3	
29495436-5	2018	In the present study, tunicamycin, an N-glycosyltransferase inhibitor, was employed to treat CHO cells (CHO-CRT) stably expressing full-length recombinant mouse CRT in secreted form for preparation of aberrantly glycosylated eCRT (tun-eCRT).	Tunicamycin	22-33	calreticulin	Homo sapiens	108-111	
24807724-5	2014	CRT was also found to be of high importance for proper oligomerization of the viral structural proteins VP26 and VP28, and when CRT glycosylation was blocked with tunicamycin, a significant decrease in both viral replication and assembly was detected.	Tunicamycin	163-174	calreticulin	Homo sapiens	128-131	
21151176-6	2011	The combination of ER stress inducers (such as THAPS or tunicamycin) and CDDP effectively induced the translocation of CRT to the plasma membrane, as well as immunogenic cell death, although ER stress or CDDP alone was insufficient to induce CRT exposure and immunogenic cell death.	Tunicamycin	56-67	calreticulin	Homo sapiens	119-122	
15383281-5	2004	In cells, calreticulin oligomerization intermediates accumulate in response to conditions that induce protein misfolding (heat shock and tunicamycin treatments), and upon calcium depletion.	Tunicamycin	137-148	calreticulin	Homo sapiens	10-22	
14744598-9	2004	FR167653 also inhibited the transactivation of calreticulin stimulated by two other endoplasmic reticulum stress inducers, tunicamycin and A23187.	Tunicamycin	123-134	calreticulin	Homo sapiens	47-59	
10353723-5	1998	ER stress induced calreticulin expression in response to either thapsigargin or tunicamycin was equivalent in these cells to that seen in control, nontransfected cells, leading us to conclude that calreticulin is unlikely be involved in its own induction.	Tunicamycin	80-91	calreticulin	Homo sapiens	18-30	
10353723-6	1998	Levels of the mRNA encoding the fusion protein were also increased by tunicamycin, but not thapsigargin, suggesting that, in agreement with our previous observations, inhibition of N-linked glycosylation may increase the stability of calreticulin mRNA.	Tunicamycin	70-81	calreticulin	Homo sapiens	234-246	
10417322-10	1999	Treatment with tunicamycin (TUN) diminished the binding of MUC2 to CRT, suggesting a requirement for initial N-glycan addition during this process.	Tunicamycin	15-26	calreticulin	Homo sapiens	67-70	
9367877-6	1997	Both thapsigargin, and tunicamycin, increased calreticulin secretion from the cells, although this might be due to more than simply saturation of KDEL receptor binding.	Tunicamycin	23-34	calreticulin	Homo sapiens	46-58