PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21670312-3 2011 We showed that cell surface expression of CRT and secretion of CRT, BiP, gp96, and PDI were induced by thapsigargin (THP) treatment, which depletes ER calcium, but not by tunicamycin treatment, which inhibits protein glycosylation. Thapsigargin 103-115 calreticulin Homo sapiens 42-45 21670312-4 2011 Surface expression of CRT in viable, THP-treated fibroblasts correlated with their enhanced phagocytic uptake by bone marrow-derived dendritic cells. Thapsigargin 37-40 calreticulin Homo sapiens 22-25 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. Thapsigargin 88-100 calreticulin Homo sapiens 15-27 28778674-10 2017 CRT knockdown was able to abolish the effect of TGF-beta1 on thapsigargin (TG) -induced Ca2+ release, but had failed to reduce store-operated Ca2+ influx. Thapsigargin 61-73 calreticulin Homo sapiens 0-3 28778674-10 2017 CRT knockdown was able to abolish the effect of TGF-beta1 on thapsigargin (TG) -induced Ca2+ release, but had failed to reduce store-operated Ca2+ influx. Thapsigargin 48-50 calreticulin Homo sapiens 0-3 21670312-3 2011 We showed that cell surface expression of CRT and secretion of CRT, BiP, gp96, and PDI were induced by thapsigargin (THP) treatment, which depletes ER calcium, but not by tunicamycin treatment, which inhibits protein glycosylation. Thapsigargin 103-115 calreticulin Homo sapiens 63-66 21670312-3 2011 We showed that cell surface expression of CRT and secretion of CRT, BiP, gp96, and PDI were induced by thapsigargin (THP) treatment, which depletes ER calcium, but not by tunicamycin treatment, which inhibits protein glycosylation. Thapsigargin 117-120 calreticulin Homo sapiens 42-45 21670312-3 2011 We showed that cell surface expression of CRT and secretion of CRT, BiP, gp96, and PDI were induced by thapsigargin (THP) treatment, which depletes ER calcium, but not by tunicamycin treatment, which inhibits protein glycosylation. Thapsigargin 117-120 calreticulin Homo sapiens 63-66 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. Thapsigargin 5-17 calreticulin Homo sapiens 46-58 21151176-5 2011 Using a screening method that monitors the voyage of CRT from the ER lumen to the cell surface, we identified thapsigargin (THAPS), an inhibitor of the sarco/ER Ca(2+)-ATPase as a molecule that on its own does not stimulate CRT exposure, yet endows CDDP with the capacity to do so. Thapsigargin 110-122 calreticulin Homo sapiens 53-56 21151176-5 2011 Using a screening method that monitors the voyage of CRT from the ER lumen to the cell surface, we identified thapsigargin (THAPS), an inhibitor of the sarco/ER Ca(2+)-ATPase as a molecule that on its own does not stimulate CRT exposure, yet endows CDDP with the capacity to do so. Thapsigargin 110-122 calreticulin Homo sapiens 224-227 21151176-5 2011 Using a screening method that monitors the voyage of CRT from the ER lumen to the cell surface, we identified thapsigargin (THAPS), an inhibitor of the sarco/ER Ca(2+)-ATPase as a molecule that on its own does not stimulate CRT exposure, yet endows CDDP with the capacity to do so. Thapsigargin 124-129 calreticulin Homo sapiens 53-56 21151176-5 2011 Using a screening method that monitors the voyage of CRT from the ER lumen to the cell surface, we identified thapsigargin (THAPS), an inhibitor of the sarco/ER Ca(2+)-ATPase as a molecule that on its own does not stimulate CRT exposure, yet endows CDDP with the capacity to do so. Thapsigargin 124-129 calreticulin Homo sapiens 224-227 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. Thapsigargin 47-52 calreticulin Homo sapiens 119-122 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. Thapsigargin 47-52 calreticulin Homo sapiens 242-245 21075854-3 2011 However, in cells treated with thapsigargin, which depletes endoplasmic reticulum calcium, major histocompatibility complex class I trafficking rates are accelerated coincident with calreticulin secretion, and detection of cell-surface calreticulin is dependent on its polypeptide binding conformations. Thapsigargin 31-43 calreticulin Homo sapiens 182-194 21075854-3 2011 However, in cells treated with thapsigargin, which depletes endoplasmic reticulum calcium, major histocompatibility complex class I trafficking rates are accelerated coincident with calreticulin secretion, and detection of cell-surface calreticulin is dependent on its polypeptide binding conformations. Thapsigargin 31-43 calreticulin Homo sapiens 236-248 14744598-5 2004 In this study, FR167653 concentration-dependently inhibited the up-regulation of the calreticulin mRNA level following an endoplasmic reticulum stress induced by thapsigargin in human embryonic kidney 293 (HEK293) cells and rat phechromocytoma PC12 cells. Thapsigargin 162-174 calreticulin Homo sapiens 85-97 14744598-6 2004 The compound concentration-dependently suppressed the transactivation of luciferase by thapsigargin in a reporter assay with a calreticulin promoter-luciferase conjugated reporter vector. Thapsigargin 87-99 calreticulin Homo sapiens 127-139 14744598-7 2004 SB203580 also significantly suppressed the transactivation of calreticulin by thapsigargin. Thapsigargin 78-90 calreticulin Homo sapiens 62-74 10952999-2 2000 Overexpression of calreticulin, an ER luminal protein, resulted in an increased sensitivity of the cells to both thapsigargin- and staurosporine-induced apoptosis. Thapsigargin 113-125 calreticulin Homo sapiens 18-30 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. Thapsigargin 64-76 calreticulin Homo sapiens 18-30 8809046-4 1996 Perturbation of intracellular Ca2+ levels by prolonged exposure to either thapsigargin or ionomycin induced calreticulin mRNA, both in the presence and absence of extracellular Ca2+, consistent with the proposal that sustained depletion of the ER Ca2+ store can trigger these increases. Thapsigargin 74-86 calreticulin Homo sapiens 108-120 32323496-5 2020 We find here that calreticulin is upregulated in human ischemic heart failure cardiac tissue, as well as simulated hypoxia and reoxygenation (H/R) and thapsigargin-mediated ER stress. Thapsigargin 151-163 calreticulin Homo sapiens 18-30 32323496-7 2020 It was found that overexpression of calreticulin promotes apoptosis, while a partial knockdown protects against the expression of caspase 12, CHOP, and reduces thapsigargin-driven TUNEL staining. Thapsigargin 160-172 calreticulin Homo sapiens 36-48