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