PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17762183-8	2007	These results show that the alkaline sondition (pH=8.0) induces cell apoptosis by activating caspase-8, which cleaves Bid to tBid, tBid translocation to mitochondria, and then activating the caspase-3 in the ASTC-a-1 cells.	tBID	125-129	caspase 3	Homo sapiens	191-200	
17762183-8	2007	These results show that the alkaline sondition (pH=8.0) induces cell apoptosis by activating caspase-8, which cleaves Bid to tBid, tBid translocation to mitochondria, and then activating the caspase-3 in the ASTC-a-1 cells.	tBID	131-135	caspase 3	Homo sapiens	191-200	
15324812-5	2004	These compounds represent the first antiapoptotic small molecules targeting a Bcl-2 protein as shown by their ability to inhibit tBid-induced SMAC release, caspase-3 activation, and cell death.	tBID	129-133	caspase 3	Homo sapiens	156-165	
16407197-3	2006	We utilized a recombinant fluorescence resonance energy transfer (FRET) Bid probe to determine the kinetics of Bid cleavage and tBid translocation during death receptor-induced apoptosis in caspase 3-deficient MCF-7 cells.	tBID	128-132	caspase 3	Homo sapiens	190-199	
23019260-6	2012	Bid in the PD temporal cortex could be further cleaved into tBid in the cytosol, which is translocated into the mitochondria, where cytochrome c is then released and caspase-3 is subsequently activated.	tBID	60-64	caspase 3	Homo sapiens	166-175	
32345661-5	2020	tBid-induced mitochondrial outer membrane permeabilization was also required to drive SMAC release and relieve inhibitor of apoptosis protein inhibition of caspase-3, thereby allowing caspase-3 auto-processing to the fully active p17/p12 form.	tBID	0-4	caspase 3	Homo sapiens	156-165	
32345661-5	2020	tBid-induced mitochondrial outer membrane permeabilization was also required to drive SMAC release and relieve inhibitor of apoptosis protein inhibition of caspase-3, thereby allowing caspase-3 auto-processing to the fully active p17/p12 form.	tBID	0-4	caspase 3	Homo sapiens	184-193	
26943324-3	2016	We observed that apoptotic cell death induced by expression of the truncated form of BH3 interacting-domain death agonist (tBid) and a constitutively active form of caspase 3 (revC3), respectively, showed higher immunogenicity than cell death induced by expression of the tuberculosis-necrotizing toxin (TNT).	tBID	123-127	caspase 3	Homo sapiens	165-174	
21704663-4	2011	The engineered polyplexes exhibited favourable physicochemical characteristics for transfection and dramatically elevated the level of Bid/tBid expression in both MUC1 over-expressing caspase 3-deficient (MCF7 cells) and caspase 3-positive (T47D and SKBR3) tumour cell lines and, concomitantly, induced considerable cell death.	tBID	139-143	caspase 3	Homo sapiens	184-193	
17520191-2	2007	Activated tBid can induce Bax oligomerization and translocation to mitochondria, triggering the release of cytochrome c, caspase-3 activation and cell apoptosis.	tBID	10-14	caspase 3	Homo sapiens	121-130