PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15117953-3 2004 We report here that the BH3-only Bcl-2 family member Bid is required for mitochondrial permeabilization and apoptosis induction by etoposide and gamma-radiation in p53 mutant T leukemic cells. Etoposide 131-140 BH3 interacting domain death agonist Homo sapiens 53-56 18373075-0 2008 Bid exhibits S phase checkpoint activation and plays a pro-apoptotic role in response to etoposide-induced DNA damage in hepatocellular carcinoma cells. Etoposide 89-98 BH3 interacting domain death agonist Homo sapiens 0-3 18373075-2 2008 The role of Bid in etoposide-induced-DNA damage in HCC has not been investigated. Etoposide 19-28 BH3 interacting domain death agonist Homo sapiens 12-15 18373075-4 2008 Upon the administration of a high dose of etoposide (causing irreparable damage), Bid sensitized cells to apoptosis. Etoposide 42-51 BH3 interacting domain death agonist Homo sapiens 82-85 18373075-5 2008 However, at a low dose of etoposide (repairable damage), Bid activated the S phase checkpoint through the up-regulation of p21 and p27, which are both p53-independent. Etoposide 26-35 BH3 interacting domain death agonist Homo sapiens 57-60 18373075-7 2008 In conclusion, our study demonstrates that Bid both exhibits S phase checkpoint activation and plays a pro-apoptotic role in response to different degrees of etoposide-induced DNA damage in HCC cells. Etoposide 158-167 BH3 interacting domain death agonist Homo sapiens 43-46 17585339-4 2007 Here, we demonstrate that etoposide and ionizing radiation induce the exit of BID from the nucleus and that leptomycin B, a specific inhibitor of the nuclear export receptor CRM1, prevents the nuclear exit of BID. Etoposide 26-35 BH3 interacting domain death agonist Homo sapiens 78-81 17585339-4 2007 Here, we demonstrate that etoposide and ionizing radiation induce the exit of BID from the nucleus and that leptomycin B, a specific inhibitor of the nuclear export receptor CRM1, prevents the nuclear exit of BID. Etoposide 26-35 BH3 interacting domain death agonist Homo sapiens 209-212 10749135-0 2000 The role of Apaf-1, caspase-9, and bid proteins in etoposide- or paclitaxel-induced mitochondrial events during apoptosis. Etoposide 51-60 BH3 interacting domain death agonist Homo sapiens 35-38 11861801-4 2002 Pretreatment with a broad caspase inhibitor [benzyloxycarbonyl-Val-Ala-Asp-(Ome) fluoromethyl ketone] markedly decreased the incidence of apoptotic cells induced by FTY720, etoposide, and anti-Fas antibody, through the abrogation of cleavage of Bid, poly(ADP-ribose) polymerase, and caspases 3, 8, and 9. Etoposide 173-182 BH3 interacting domain death agonist Homo sapiens 245-248 11784858-15 2002 Moreover, in etoposide-treated cells, Hsp27 still delayed the release of cytochrome c from mitochondria and Bid intracellular redistribution in conditions where F-actin was not altered. Etoposide 13-22 BH3 interacting domain death agonist Homo sapiens 108-111 10822279-4 2000 Here, we show that BID is cleaved in response to multiple death-inducing stimuli (staurosporine, UV radiation, cycloheximide, etoposide). Etoposide 126-135 BH3 interacting domain death agonist Homo sapiens 19-22 9400949-16 1997 The recommended dose for use in phase II clinical trials is topotecan 1.0 mg m-2 on days 1-5 and etoposide 40 mg bid on days 6-12 every 4 weeks. Etoposide 97-106 BH3 interacting domain death agonist Homo sapiens 113-116 23093908-13 2012 CONCLUSION: Taken together, these results suggest that overexpression of Bid suppressed the activation of Akt, p38, and c-Jun, and promoted the activation of ERK1/2 induced by etoposide, suggesting that the promotion of ERK1/2 activation may have a negative effect on Bid-mediated HCC DNA damage induced by etoposide. Etoposide 176-185 BH3 interacting domain death agonist Homo sapiens 268-271 23093908-0 2012 Bid-overexpression regulates proliferation and phosphorylation of Akt and MAPKs in response to etoposide-induced DNA damage in hepatocellular carcinoma cells. Etoposide 95-104 BH3 interacting domain death agonist Homo sapiens 0-3 23093908-2 2012 However, the effects of Bid on hepatocellular carcinoma (HCC) cell proliferation in response to etoposide-induced DNA damage have not been sufficiently investigated. Etoposide 96-105 BH3 interacting domain death agonist Homo sapiens 24-27 23093908-3 2012 METHODS: Using a stable Bid-overexpression HCC cell line, Bid/PLC/PRF/5, overexpression of Bid promoted loss of viability in response to etoposide-induced DNA damage. Etoposide 137-146 BH3 interacting domain death agonist Homo sapiens 24-27 23093908-3 2012 METHODS: Using a stable Bid-overexpression HCC cell line, Bid/PLC/PRF/5, overexpression of Bid promoted loss of viability in response to etoposide-induced DNA damage. Etoposide 137-146 BH3 interacting domain death agonist Homo sapiens 58-61 23093908-3 2012 METHODS: Using a stable Bid-overexpression HCC cell line, Bid/PLC/PRF/5, overexpression of Bid promoted loss of viability in response to etoposide-induced DNA damage. Etoposide 137-146 BH3 interacting domain death agonist Homo sapiens 58-61 23093908-6 2012 RESULTS: The survival rates of 100 muM etoposide on the cells with control vector and Bid/PLC/PRF/5 at 48 hours amounted to 71% +- 0.75% and 59% +- 0.60% with MTT assay, and similar results of 85% +- 0.08% and 63% +- 0.14% with BrdU-labeling assay respectively. Etoposide 39-48 BH3 interacting domain death agonist Homo sapiens 86-89 23093908-7 2012 Moreover, overexpression of Bid sensitized the cells to apoptosis at a high dose of etoposide (causing irreparable damage). Etoposide 84-93 BH3 interacting domain death agonist Homo sapiens 28-31 23093908-10 2012 Overexpression of Bid suppressed the activation of Akt with respect to etoposide-induced DNA damage. Etoposide 71-80 BH3 interacting domain death agonist Homo sapiens 18-21 23093908-13 2012 CONCLUSION: Taken together, these results suggest that overexpression of Bid suppressed the activation of Akt, p38, and c-Jun, and promoted the activation of ERK1/2 induced by etoposide, suggesting that the promotion of ERK1/2 activation may have a negative effect on Bid-mediated HCC DNA damage induced by etoposide. Etoposide 176-185 BH3 interacting domain death agonist Homo sapiens 73-76 23124518-3 2012 In addition, sequential treatment with etoposide and TRAIL increased caspases 8, 9 and 3 activation, Mcl-1 cleavage and Bid truncation, which suggests that the ability of etoposide and TRAIL to induce apoptosis is mediated through activation of an intrinsic signalling pathway. Etoposide 39-48 BH3 interacting domain death agonist Homo sapiens 120-123 23124518-3 2012 In addition, sequential treatment with etoposide and TRAIL increased caspases 8, 9 and 3 activation, Mcl-1 cleavage and Bid truncation, which suggests that the ability of etoposide and TRAIL to induce apoptosis is mediated through activation of an intrinsic signalling pathway. Etoposide 171-180 BH3 interacting domain death agonist Homo sapiens 120-123 23093908-13 2012 CONCLUSION: Taken together, these results suggest that overexpression of Bid suppressed the activation of Akt, p38, and c-Jun, and promoted the activation of ERK1/2 induced by etoposide, suggesting that the promotion of ERK1/2 activation may have a negative effect on Bid-mediated HCC DNA damage induced by etoposide. Etoposide 307-316 BH3 interacting domain death agonist Homo sapiens 73-76 21801448-9 2011 Finally, the caspase-9 inhibitor Ac-LEHD-CHO or caspase-9 siRNA blocked etoposide-induced caspase-8 activation, Bid cleavage, and apoptosis in both cell lines, indicating that p53/p73-dependent caspase-8 activation lies downstream of mitochondria. Etoposide 72-81 BH3 interacting domain death agonist Homo sapiens 112-115 20025574-0 2009 Association of p53 with Bid induces cell death in response to etoposide treatment in hepatocellular carcinoma. Etoposide 62-71 BH3 interacting domain death agonist Homo sapiens 24-27 21468663-9 2011 Moreover, the pretreatment with trichostatin A (TSA, a histone deacetylase inhibitor) or TSA in combination with etoposide significantly sensitized HCC cells to apoptosis by inhibiting ERK phosphorylation, reactivating caspases and PARP, and inducing translocation of p53 and Bid to cytoplasm. Etoposide 113-122 BH3 interacting domain death agonist Homo sapiens 276-279 21468663-4 2011 In this study, we showed that etoposide treatment activated caspase-8 and caspase-3, leading to cleavages of p53, Bid and PARP, which subsequently induced apoptosis. Etoposide 30-39 BH3 interacting domain death agonist Homo sapiens 114-117 21468663-5 2011 Furthermore, p53 and Bid were accumulated in cytoplasm following etoposide treatment. Etoposide 65-74 BH3 interacting domain death agonist Homo sapiens 21-24 20025574-6 2009 Here, we showed that etoposide-induced DNA damage could significantly induce p53 and Bid nuclear export. Etoposide 21-30 BH3 interacting domain death agonist Homo sapiens 85-88 20025574-7 2009 When cells were stimulated by etoposide, p53 could, through the association with Bid, cause translocation of Bid from the nucleus to the cytoplasm and on to its ultimate location in the mitochondria. Etoposide 30-39 BH3 interacting domain death agonist Homo sapiens 81-84 20025574-7 2009 When cells were stimulated by etoposide, p53 could, through the association with Bid, cause translocation of Bid from the nucleus to the cytoplasm and on to its ultimate location in the mitochondria. Etoposide 30-39 BH3 interacting domain death agonist Homo sapiens 109-112 20025574-8 2009 p53 was physically associated with Bid, and both p53 and Bid cooperatively promoted cell death induced by etoposide. Etoposide 106-115 BH3 interacting domain death agonist Homo sapiens 57-60 20025574-9 2009 Knockdown of Bid expression notably attenuated cell death induced by etoposide and also released p53 from the mitochondria. Etoposide 69-78 BH3 interacting domain death agonist Homo sapiens 13-16 20025574-10 2009 These findings reveal a novel mechanism by which p53 is associated with Bid in the nucleus to facilitate exportation of Bid to the mitochondria and induce apoptosis in response to etoposide-induced DNA damage in HCC. Etoposide 180-189 BH3 interacting domain death agonist Homo sapiens 72-75 20025574-10 2009 These findings reveal a novel mechanism by which p53 is associated with Bid in the nucleus to facilitate exportation of Bid to the mitochondria and induce apoptosis in response to etoposide-induced DNA damage in HCC. Etoposide 180-189 BH3 interacting domain death agonist Homo sapiens 120-123 19233849-3 2009 Cells stably depleted of Bid were far less sensitive than control-transfected cells to etoposide-induced apoptosis. Etoposide 87-96 BH3 interacting domain death agonist Homo sapiens 25-28 18665234-6 2008 While Bid-deficient cells were equally sensitive to ER stress-induced apoptosis, they showed moderate, but significantly reduced levels of apoptosis, as well as increased clonogenic survival in response to the genotoxic drugs Etoposide, Oxaliplatin, and Doxorubicin. Etoposide 226-235 BH3 interacting domain death agonist Homo sapiens 6-9 18665234-8 2008 Interestingly, Bid-deficient cells were dramatically protected from apoptosis when subtoxic concentrations of ER stressors, Etoposide or Oxaliplatin were combined with subtoxic TRAIL concentrations. Etoposide 124-133 BH3 interacting domain death agonist Homo sapiens 15-18