PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21423217-0 2011 Bid can mediate a pro-apoptotic response to etoposide and ionizing radiation without cleavage in its unstructured loop and in the absence of p53. Etoposide 44-53 BH3 interacting domain death agonist Mus musculus 0-3 21423217-4 2011 Bid has also been implicated in the apoptotic response to ionizing radiation (IR) and the topoisomerase inhibitor etoposide, anti-cancer regimens that cause double-strand (ds)DNA breaks. Etoposide 114-123 BH3 interacting domain death agonist Mus musculus 0-3 21423217-7 2011 We used Bid-deficient mouse embryonic fibroblast (MEF) lines that were reconstituted with Bid to control the cellular background and demonstrated that the Bid-dependent apoptotic pathway induced by IR and etoposide operates in MEFs that are transformed by SV40, but is not evident in E1A/Ras-transformed MEFs. Etoposide 205-214 BH3 interacting domain death agonist Mus musculus 8-11 21423217-7 2011 We used Bid-deficient mouse embryonic fibroblast (MEF) lines that were reconstituted with Bid to control the cellular background and demonstrated that the Bid-dependent apoptotic pathway induced by IR and etoposide operates in MEFs that are transformed by SV40, but is not evident in E1A/Ras-transformed MEFs. Etoposide 205-214 BH3 interacting domain death agonist Mus musculus 90-93 21423217-7 2011 We used Bid-deficient mouse embryonic fibroblast (MEF) lines that were reconstituted with Bid to control the cellular background and demonstrated that the Bid-dependent apoptotic pathway induced by IR and etoposide operates in MEFs that are transformed by SV40, but is not evident in E1A/Ras-transformed MEFs. Etoposide 205-214 BH3 interacting domain death agonist Mus musculus 90-93 21423217-9 2011 In these cells, Bid acted in a conventional manner in that it required its BH3 domain to mediate apoptosis in response to IR and etoposide, and triggered apoptotic execution by indirect activation of Bak/Bax, mitochondrial permeabilization and caspase-9 activation. Etoposide 129-138 BH3 interacting domain death agonist Mus musculus 16-19 21423217-10 2011 However, the mechanism of Bid activation was unconventional, because elimination of all known or suspected cleavage sites for caspases or other proteolytic enzymes and even complete elimination of its unstructured cleavage loop left Bid"s pro-apoptotic role in the response to IR and etoposide unaffected. Etoposide 284-293 BH3 interacting domain death agonist Mus musculus 26-29 16122426-5 2005 In contrast, introducing a nonphosphorylatable BID mutant did not restore accumulation in the S phase and resulted in an increase in cellular sensitivity to etoposide-induced apoptosis. Etoposide 157-166 BH3 interacting domain death agonist Mus musculus 47-50